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BIOMARKER:

NOTCH1 expression

i
Other names: NOTCH1, TAN1
Entrez ID:
Related biomarkers:
21h
Mechanistic studies revealed that KLF9 reduced the transcriptional expression of Notch1 by directly binding to Notch1 promoter, thereby inhibited function of slug in a CSL-dependent manner. Clinically, expression of KLF9 was associated with histological grade and loss of KLF9 predicts poor prognosis in OC.
Journal
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KIT (KIT proto-oncogene, receptor tyrosine kinase) • NOTCH1 (Notch 1) • CD44 • SNAI2 (Snail Family Transcriptional Repressor 2)
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NOTCH1 expression
27d
Lastly, knockdown of Nrf2 increased the sensitivity of anaplastic thyroid cancer cells to lenvatinib. As knockdown of Nrf2 reduced the metastatic and invasive ability of anaplastic thyroid cancer cells by inhibiting the Notch 1 signaling pathway and increased the cancer cell sensitivity to lenvatinib, Nrf2 could be a promising therapeutic target for patients with anaplastic thyroid cancer.
Journal
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NOTCH1 (Notch 1)
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NOTCH1 expression
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lenvatinib
1m
Proving the role of Notch, the ectopic expression of the activated Notch1 intracellular domain rescued G9-induced effects. This work supports the potential of USP9x inhibition to target Notch in metabolically vulnerable tissues like TNBC, while sparing normal Notch-dependent tissues.
Journal
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NOTCH1 (Notch 1) • CCL2 (Chemokine (C-C motif) ligand 2) • IL1B (Interleukin 1, beta)
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NOTCH1 expression
1m
Expectedly, targeted overexpression miR-139 or PDE2A in glioma with OCP system significantly repressed the stemness and decelerated glioma progression. Our findings elaborate on the inhibitory functions of PDE2A and miR-139 on GSC stemness and tumorigenesis, which may provide new prognostic markers and therapeutic targets for GBMs.
Journal
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NOTCH1 (Notch 1) • HES1 • MIR139 (MicroRNA 139)
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NOTCH1 expression
1m
Forced activation of Notch signaling pathway successfully rescues the growth, migration, and invasion capacities of METTL3-depleted ESCC cells. Our data uncovered important mechanistical insights underlying ESCC tumorigenesis and provided molecular basis for the development of novel strategies for ESCC diagnosis and treatment.
Journal
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NOTCH1 (Notch 1) • METTL3 (Methyltransferase Like 3)
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NOTCH1 expression
1m
In summary, our results revealed that Notch1 activation by doxycycline induces S phase arrest, apoptosis and autophagy by blocking PI3K/Akt/mTOR signalling in human osteosarcoma cells. Notch1 may be a potential clinical antitumour target for osteosarcoma therapy.
Journal
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NOTCH1 (Notch 1) • AKT1 (V-akt murine thymoma viral oncogene homolog 1)
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NOTCH1 expression
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doxycycline
1m
Interaction between Notch1 and TAZ promoted aerobic glycolysis and immune escape in lung cancer. Our findings provide potential therapeutic targets against Notch1 and TAZ and would be important for clinical translation in lung cancer.
Journal
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NOTCH1 (Notch 1)
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NOTCH1 expression
1m
These data indicated that the level of HER3 is regulated by NOTCH1 in SCCHN both transcriptionally and post-translationally, and NOTCH1 is in a higher hierarchy in the regulatory system of the AKT pathway. Since NOTCH1 is inactivated in approximately 10% of SCCHN cases and this aberration strongly impacts the AKT pathway and diminishes HER3, exclusion of patients with NOTCH1-inactivated SCCHN may be beneficial for future clinical trials of HER3-targeting antibodies.
Journal • PD(L)-1 Biomarker • IO biomarker
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HER-2 (Human epidermal growth factor receptor 2) • NOTCH1 (Notch 1) • NRG1 (Neuregulin 1) • ERBB3 (V-erb-b2 avian erythroblastic leukemia viral oncogene homolog 3)
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ERBB3 expression • ERBB3 overexpression • NOTCH1 expression
2ms
The gene expression analysis further revealed that rutin treatment decreases Notch-1 and Hes-1 mRNA expression. Altogether, these results showed that rutin showed potent anticancer effects in human cervical cancer Caski cells by triggering apoptosis, G0/G1 phase arrest, and downregulating the level of Notch-1 and Hes-1 of the Notch signaling pathway.
Journal • IO biomarker
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BCL2 (B-cell CLL/lymphoma 2) • NOTCH1 (Notch 1) • CCND1 (Cyclin D1) • CDK4 (Cyclin-dependent kinase 4) • BAX (BCL2-associated X protein) • CASP3 (Caspase 3) • HES1 • CASP9 (Caspase 9)
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BCL2 expression • CCND1 expression • NOTCH1 expression • CCND1 expression + CDK4 expression • NOTCH1 overexpression
2ms
Additionally, phorbol 12-myristate 13-acetate was used to activate PLC, and Jagged1 was used as a Notch activator to verify whether metformin could suppress CRPC development via the PLCε/Notch1/AR pathways. The results confirmed that metformin may serve critical roles in CRPC by significantly inhibiting the occurrence, growth and proliferation of CRPC tumors by decreasing PLCε/Notch1 expression and AR nucleation.
Preclinical • Journal
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NOTCH1 (Notch 1) • HES1
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NOTCH1 expression
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metformin
2ms
Hsa-miR-599 expression is downregulated in breast cancer. Hsa-miR-599 may inactivate BRD4/Jagged1/Notch1 axis, thus suppressing malignant progression of breast cancer.
Journal
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NOTCH1 (Notch 1) • BRD4 (Bromodomain Containing 4)
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NOTCH1 expression
2ms
Our findings suggest that SIRT1 is a promising target in T-ALL and offer a mechanistic link between the upregulation of SIRT1 and downregulation of p27.
Journal
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NOTCH1 (Notch 1) • CDK2 (Cyclin-dependent kinase 2) • SKP2 (S-phase kinase-associated protein 2)
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NOTCH1 expression • SIRT1 overexpression • CDK2 expression
2ms
These findings indicate that the MAPK pathway is activated in dasatinib-resistant uterine cancer cells and that EphrinA1-mediated MEK inhibition overcomes dasatinib resistance. Dual targeting of both EphA2 and MEK, combined with chemotherapy, should be considered for future clinical development.
Journal
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BRAF (B-raf proto-oncogene) • MYC (V-myc avian myelocytomatosis viral oncogene homolog) • NOTCH1 (Notch 1) • NOTCH3 (Notch Receptor 3) • HES1
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MYC expression • NOTCH1 expression • NOTCH3 expression
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Mekinist (trametinib) • dasatinib • carboplatin • paclitaxel
2ms
Taken together, these results indicated that HeLa-229PTR cells develop the EMT phenotype partly through activation of Notch1 signaling. Thus, inhibition of Notch1 signaling can be a strategy for the reversal of the EMT phenotype and may increase the sensitivity of cervical cancer cells to treatment with paclitaxel.
Journal
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NOTCH1 (Notch 1)
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NOTCH1 expression
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paclitaxel
2ms
The proliferation of U87-MG and LN229 was not significantly suppressed after transfection with Notch siRNA. These results demonstrated that propranolol suppressed the proliferation of glioblastoma cell lines and neuroblastoma cell line, and Hes1 was more closely involved than Notch1 was in glioblastoma proliferation.
Preclinical • Journal
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NOTCH1 (Notch 1) • HES1
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NOTCH1 expression
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propranolol
2ms
In addition, RUSC1-AS1 functioned as a competing endogenous RNA (ceRNA) to competitively sponge miR-101-3p, thus upregulating Notch1 expression and mediating the malignant behaviors of OS cells. RUSC1-AS1 is a novel oncogenic lncRNA in OS through the miR-101-3p-Notch1-Ras-ERK pathway, which might be a potential therapeutic target for OS.
Journal
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NOTCH1 (Notch 1) • CDH1 (Cadherin 1) • VIM (Vimentin)
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CDH1 expression • NOTCH1 expression • VIM expression
2ms
In addition, we identified APOL1 could be a regulator of NOTCH1 signaling pathway using bioinformatics tools, qRT-PCR, dual-luciferase reporter assay, and western blotting. In summary, APOL1 could function as an oncogene to promote proliferation and inhibit apoptosis through activating NOTCH1 signaling pathway expression in pancreatic cancer; therefore, it may act as a novel therapeutic target for pancreatic cancer.
Journal
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NOTCH1 (Notch 1)
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NOTCH1 expression
2ms
In addition, the Notch1/Hes1 pathway inhibitor DAPT significantly downregulated the expression of FOXP3 in a dose-dependent manner. Taken together, these findings demonstrated that FOXP3 may facilitate the invasive and migratory abilities of NSCLC cells via regulating the angiogenic factor VEGF, the EMT and the Notch1/Hes1 pathway.
Journal
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NOTCH1 (Notch 1) • CDH1 (Cadherin 1) • CD31 (Platelet and endothelial cell adhesion molecule 1) • HES1 • MMP2 (Matrix metallopeptidase 2) • VIM (Vimentin) • MMP9 (Matrix metallopeptidase 9) • FOXP3 (Forkhead Box P3)
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CDH1 expression • CD31 expression • NOTCH1 expression • VIM expression • FOXP3 expression
2ms
Analysis of 233 primary and 40 recurrent HNSCC cancer biopsies revealed that high DCLK1 expression was associated with poor prognosis and showed a trend towards higher active NOTCH1 expression in tumors with elevated DCLK1. Our results demonstrate the novel role of DCLK1 as a regulator of NOTCH signaling network and suggest its potential as a therapeutic target in HNSCC.
Journal
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NOTCH1 (Notch 1) • HES1
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NOTCH1 expression
3ms
Collectively, this study provides evidence for the effectiveness of P. capillacea and C. officinalis polysaccharides in targeting BCSCs through interfering with substantial signaling pathways contributing to their functionality.
Journal
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MYC (V-myc avian myelocytomatosis viral oncogene homolog) • NOTCH1 (Notch 1) • CCND1 (Cyclin D1) • CD44 • CD24 (CD24 Molecule) • POU5F1 (POU Class 5 Homeobox 1) • SOX2 • HES1 • VIM (Vimentin) • ALDH1A1 (Aldehyde Dehydrogenase 1 Family Member A1)
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CCND1 expression • NOTCH1 expression
3ms
The antitumor properties and regulatory effect of DAPT against the extracellular matrix (ECM) and Hes1/PTEN/AKT/mTOR signaling were verified by the HepG2 xenograft experiments. DAPT could suppress the proliferation and migration of HCC by regulating the ECM and inhibiting the Hes1/PTEN/AKT/mTOR signaling pathway.
Journal
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PTEN (Phosphatase and tensin homolog) • NOTCH1 (Notch 1) • HES1 • MMP9 (Matrix metallopeptidase 9)
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NOTCH1 expression
3ms
After treatment with PTX, apoptosis and ROS levels were decreased in the CD44CD117 groups compared with the CD44CD117 groups. Collectively, the present results demonstrated that, via the Notch1 pathway, CCL20/CCR6 may promote the stemness and PTX resistance of CD44CD117 cells in ovarian cancer.
Journal
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KIT (KIT proto-oncogene, receptor tyrosine kinase) • NOTCH1 (Notch 1) • CD44 • POU5F1 (POU Class 5 Homeobox 1) • CCL20 (C-C Motif Chemokine Ligand 20)
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NOTCH1 expression • POU5F1 expression
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paclitaxel
3ms
In addition, we used data from TCGA to show that putative inactivating NOTCH1 mutations co-occur with KRAS mutations and genomic amplifications in lung adenocarcinomas. Our in vivo study provides evidence that Notch1 deficiency in mutated Kras driven lung carcinomas contributes to lung carcinogenesis in a subgroup of patients by increasing TAZ expression who might benefit from TAZ signaling blockade.
Preclinical • Journal
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KRAS (KRAS proto-oncogene GTPase) • NOTCH1 (Notch 1)
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KRAS mutation • NOTCH1 mutation • NOTCH1 expression • KRAS deletion • NOTCH1 deletion • KRAS expression
3ms
The therapeutic effects were demonstrated to be dose dependent. In conclusion, the findings of the study showed that ETSJC improved the chemosensitivity of 5-FU by blocking Notch1/Hes1 signaling pathway in gastric cancer-bearing mice.
Preclinical • Journal • IO biomarker
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BCL2 (B-cell CLL/lymphoma 2) • NOTCH1 (Notch 1) • BAX (BCL2-associated X protein) • CASP3 (Caspase 3) • CD31 (Platelet and endothelial cell adhesion molecule 1) • HES1
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BCL2 expression • BAX expression • CD31 expression • NOTCH1 expression
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5-fluorouracil
3ms
Dual-luciferase assay demonstrated that DLX5 specifically activates the NOTCH1 promoter and controls its expression. Taken together, our results support that DLX5 plays an oncogenic role in OS development, which can at least partially, be attributed to activation of the NOTCH signaling pathway.
Journal
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MYC (V-myc avian myelocytomatosis viral oncogene homolog) • NOTCH1 (Notch 1) • HES1
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MYC expression • NOTCH1 expression • NOTCH1 overexpression
3ms
Results Compared with the control group, PNS could inhibit the proliferation of U2OS cells and the formation of clonal plaques, increase cell apoptosis rate, weaken the ability of migration and invasion and decrease the expression levels of Notch1 and Hes1 in the cells in a dose-dependent manner. Conclusion PNS can significantly inhibit the proliferation, migration and invasion and promote cell apoptosis of U2OS cells by blocking Notch1 signaling pathway.
Journal
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NOTCH1 (Notch 1) • HES1
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NOTCH1 expression
3ms
EGFR, PIK3CA, and FGFR3 somatic mutations were found by next-generation sequencing in 56% of the cases. We consider that cutaneous lymphadenoma is a distinct benign lymphoepithelial tumor with androgen receptor and hair follicle bulge stem cell marker expression, RS-L cell-derived Notch1 ligand, and common EGFR gene mutations.
Journal
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EGFR (Epidermal growth factor receptor) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • FGFR3 (Fibroblast growth factor receptor 3) • AR (Androgen receptor) • NOTCH1 (Notch 1) • TNFRSF8 (TNF Receptor Superfamily Member 8) • CD4 (CD4 Molecule) • FOXP3 (Forkhead Box P3) • NKX3-1 (NK3 homeobox 1)
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EGFR mutation • PIK3CA mutation • FGFR3 mutation • TNFRSF8 expression • NOTCH1 expression
4ms
This study provides novel insights into CLL relapse biology and pathways associated with known and novel biomarkers for relapse and overall survival. The modules associated with relapse and overall survival represented both known and novel pathways associated with CLL pathogenesis and can be a resource for the CLL research community. The hub genes of these modules, e.g., ARHGAP27P2, C1S, CASC2, CLEC3B, CRY1, CXCR5, FUT5, MID1IP1, and URAHP, can be studied further as new therapeutic targets or clinical markers to predict CLL patient outcomes.
Clinical • Journal • IO biomarker
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TP53 (Tumor protein P53) • BCL2 (B-cell CLL/lymphoma 2) • NOTCH1 (Notch 1) • SF3B1 (Splicing Factor 3b Subunit 1) • CD19 (CD19 Molecule) • CD5 (CD5 Molecule) • CRY1, Cryptochrome Circadian Regulator 1, • CXCR5 (C-X-C Motif Chemokine Receptor 5)
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SF3B1 mutation • NOTCH1 expression
4ms
Furthermore, the Notch pathway activator Jagged-1/FC reversed the effects of palbociclib on cell proliferation, apoptosis, senescence and cell cycle progression. These findings demonstrated that palbociclib could inhibit proliferation and induce senescence, cell cycle arrest and apoptosis in GC cells by inhibiting the Notch pathway.
Journal • IO biomarker
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BCL2 (B-cell CLL/lymphoma 2) • NOTCH1 (Notch 1) • NOTCH2 (Notch 2) • BAX (BCL2-associated X protein) • CASP3 (Caspase 3) • HES1 • CDKN1A (Cyclin-dependent kinase inhibitor 1A)
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BCL2 expression • BAX expression • NOTCH1 expression
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Ibrance (palbociclib)
4ms
C-kit PLCs had the characteristics of tumor stem cells and were more sensitive to chemotherapy drugs.
Journal
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NOTCH1 (Notch 1) • ABCB1 (ATP Binding Cassette Subfamily B Member 1) • CTNNB1 (Catenin (cadherin-associated protein), beta 1) • ABCG2 • CDH1 (Cadherin 1) • GPC3 (Glypican 3) • BMI1 (BMI1 proto-oncogene, polycomb ring finger) • EPCAM (Epithelial cell adhesion molecule) • POU5F1 (POU Class 5 Homeobox 1) • SOX2 • NANOG (Nanog Homeobox) • NES (Nestin)
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KIT expression • CDH1 expression • NOTCH1 expression • BMI1 expression • POU5F1 expression
4ms
Activation of NOTCH2 and JAGGED1 expression might also influence clinical outcomes in this group, indicating the need for further dedicated studies. The evaluation of different NOTCH network components might represent a new approach to refine CLL risk stratification.
Journal
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NOTCH1 (Notch 1) • IGH (Immunoglobulin Heavy Locus) • NOTCH2 (Notch 2)
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NOTCH1 mutation • IGH mutation • NOTCH1 expression
4ms
Altogether, our study demonstrates that NOTCH and YAP concomitant activation is frequent in human cholangiocarcinogenesis. NOTCH and YAP synergize to promote iCCA formation by activating the mTORC1 pathway.
Preclinical • Journal
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NOTCH1 (Notch 1)
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NOTCH1 expression • NOTCH1 overexpression
4ms
In the present study, we investigated the influence of the Notch1 activity level on the pharmacological interaction between cisplatin (CDDP) and two HDIs, valproic acid (VPA) and suberoylanilide hydroxamic acid (SAHA, vorinostat), in luminal-like BC cells. Therefore, treatment of CDDP with HDIs could be used to optimize a combined therapy based on CDDP against Notch1-altered luminal BC. In conclusion, the combined therapy of HDIs and CDDP may be a promising therapeutic tool in the treatment of luminal-type BC with altered Notch1 activity.
Journal • Epigenetic controller
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NOTCH1 (Notch 1)
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NOTCH1 expression
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cisplatin • Zolinza (vorinostat)
4ms
In contrast, lnc-MEG3 was downregulated in chronic ITP patients compared to healthy controls, and lower expression levels were significantly associated with poor prognosis and refractory disease phenotype. Conclusions : Lnc-MEG3 and lnc-NOTCH1 are independent non-invasive prognostic biomarker in chronic ITP, hence they could be therapeutically targeted in future.
NOTCH1 (Notch 1)
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NOTCH1 expression
5ms
In Rbpj-deficient ECs generated by CRISPR-Cas9 technology, N1ICD is unable to induce CXCL2 expression. Conclusion In summary, ovarian cancer cells employ the tumor endothelium to secrete CXCL2 in order to facilitate an immunosuppressive microenvironment.
NOTCH1 (Notch 1) • CD74 (CD74 Molecule)
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NOTCH1 expression • CD74 expression
5ms
In Rbpj-deficient ECs generated by CRISPR-Cas9 technology, N1ICD is unable to induce CXCL2 expression. Conclusion In summary, ovarian cancer cells employ the tumor endothelium to secrete CXCL2 in order to facilitate an immunosuppressive microenvironment.
NOTCH1 (Notch 1) • CD74 (CD74 Molecule)
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NOTCH1 expression • CD74 expression
5ms
In Rbpj-deficient ECs generated by CRISPR-Cas9 technology, N1ICD is unable to induce CXCL2 expression. Conclusion In summary, ovarian cancer cells employ the tumor endothelium to secrete CXCL2 in order to facilitate an immunosuppressive microenvironment.
NOTCH1 (Notch 1) • CD74 (CD74 Molecule)
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NOTCH1 expression • CD74 expression
5ms
In Rbpj-deficient ECs generated by CRISPR-Cas9 technology, N1ICD is unable to induce CXCL2 expression. Conclusion In summary, ovarian cancer cells employ the tumor endothelium to secrete CXCL2 in order to facilitate an immunosuppressive microenvironment.
NOTCH1 (Notch 1) • CD74 (CD74 Molecule)
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NOTCH1 expression • CD74 expression
5ms
Conclusion Our findings show the association of NOTCH pathway activation with a better prognosis in HNSCC patients, also revealing membranous NOTCH1 expression as a robust independent predictor of improved survival. Hence, these results suggest a tumor suppressive rather than an oncogenic role for NOTCH pathway in HNSCC.
Clinical
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NOTCH1 (Notch 1) • CCND1 (Cyclin D1) • HES1 • CDKN1A (Cyclin-dependent kinase inhibitor 1A)
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CCND1 expression • NOTCH1 expression
5ms
Conclusion Our findings show the association of NOTCH pathway activation with a better prognosis in HNSCC patients, also revealing membranous NOTCH1 expression as a robust independent predictor of improved survival. Hence, these results suggest a tumor suppressive rather than an oncogenic role for NOTCH pathway in HNSCC.
Clinical
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NOTCH1 (Notch 1) • CCND1 (Cyclin D1) • HES1 • CDKN1A (Cyclin-dependent kinase inhibitor 1A)
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CCND1 expression • NOTCH1 expression
5ms
Conclusion Our findings show the association of NOTCH pathway activation with a better prognosis in HNSCC patients, also revealing membranous NOTCH1 expression as a robust independent predictor of improved survival. Hence, these results suggest a tumor suppressive rather than an oncogenic role for NOTCH pathway in HNSCC.
Clinical
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NOTCH1 (Notch 1) • CCND1 (Cyclin D1) • HES1 • CDKN1A (Cyclin-dependent kinase inhibitor 1A)
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CCND1 expression • NOTCH1 expression
5ms
Conclusion Our findings show the association of NOTCH pathway activation with a better prognosis in HNSCC patients, also revealing membranous NOTCH1 expression as a robust independent predictor of improved survival. Hence, these results suggest a tumor suppressive rather than an oncogenic role for NOTCH pathway in HNSCC.
Clinical
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NOTCH1 (Notch 1) • CCND1 (Cyclin D1) • HES1 • CDKN1A (Cyclin-dependent kinase inhibitor 1A)
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CCND1 expression • NOTCH1 expression
5ms
Such data indicated that beta-elemene treatment attenuated the malignancy of NSCLC cells by up-regulating C3orf21 expression. Our findings may provide new mechanisms underlying the pharmacological action of beta-elemene.
Journal
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PTEN (Phosphatase and tensin homolog) • MYC (V-myc avian myelocytomatosis viral oncogene homolog) • NOTCH1 (Notch 1) • CCND1 (Cyclin D1) • MMP2 (Matrix metallopeptidase 2) • MMP9 (Matrix metallopeptidase 9)
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CCND1 expression • NOTCH1 expression
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elemene injection
5ms
Hypoxia promoted PC cell dedifferentiation to stem-like cell phenotypes with high tumorigenic potential by activating HIF-1α/Notch signaling pathway, indicating a novel role in regulating PC progression.
Journal
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NOTCH1 (Notch 1) • CXCR4 (Chemokine (C-X-C motif) receptor 4) • HIF1A (Hypoxia inducible factor 1, alpha subunit) • CD44 • NES (Nestin)
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HIF1A expression • NOTCH1 expression • NOTCH1 overexpression
5ms
In conclusion, our study suggested that NOTCH1 expression is associated with the progression of OSCC. We also demonstrated that presence of a mutated NOTCH1 gene will help prognostic stratification in OSCC when combined with other clinicopathologic parameters.
Journal
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NOTCH1 (Notch 1) • EGF (Epidermal growth factor)
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NOTCH1 mutation • NOTCH1 expression
5ms
Indeed, we found BCAT1 KD cells to be particularly sensitive to topoisomerase inhibitors such as etoposide...Genetic depletion of BCAT1 slows tumor growth in vivo and renders cells particularly sensitive to topoisomerase inhibitors. Our results identify BCAT1 as a novel therapeutic target and suggest that a combination of BCAT1 inhibitor and topoisomerase inhibitor could be particularly useful in BCAT1 overexpressing T-ALL cases.
NOTCH1 (Notch 1) • BCAT1 (Branched Chain Amino Acid Transaminase 1 )
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NOTCH1 mutation • NOTCH1 expression • BCAT1 expression • NOTCH1 overexpression
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etoposide IV
5ms
In addition, the GASC1 inhibitor caffeic acid and/or the NOTCH1 inhibitor DAPT (a γ‑Secretase Inhibitor), efficiently suppressed the human glioma xenograft tumors. Thus, the present results demonstrated the importance of GASC1 in the progression of glioma and identified that GASC1 promotes glioma progression, at least in part, by enhancing NOTCH signaling, suggesting that GASC1/NOTCH1 signaling may be a potential therapeutic target for glioma treatment.
Journal
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NOTCH1 (Notch 1) • CD133 • HES1
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NOTCH1 expression • CD133 expression • NOTCH1 overexpression
5ms
In addition, knockdown of Reck by siRNA not only mimicked miR-221/222 effects, but also demonstrated involvement of Reck in the miR-221/222-induced activation of Notch1 signaling, verifying the essential roles of the miR-221/222-Reck-Notch1 axis in regulating stemness of NSCLC cells. These findings uncover a novel mechanism by which lung CSCs are significantly manipulated by miR-221/222, and provide a potential therapeutic target for the treatment of NSCLC.
Journal
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NOTCH1 (Notch 1) • CD133 • POU5F1 (POU Class 5 Homeobox 1) • NANOG (Nanog Homeobox) • MIR221 (MicroRNA 221)
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NOTCH1 expression • POU5F1 expression
6ms
The rs2305948 and rs699947 SNPs in VEGFR2 and VEGFA, respectively, were markers of poor prognosis correlating with locoregional relapse, a higher N stage, and metastatic shedding. In conclusion, VEGF and VEGFR SNPs, miRNAs, and Notch 1 levels are potential useful biomarkers for the management of advanced CRC under regorafenib treatment.
Clinical • Journal
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NOTCH1 (Notch 1) • KDR (Kinase insert domain receptor) • FLT1 (Fms-related tyrosine kinase 1) • MIR126 (MicroRNA 126) • MIR92A1 (MicroRNA 92a-1) • miR-185 (MicroRNA 185)
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NOTCH1 expression • FLT1 expression
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Stivarga (regorafenib)
6ms
ACC is a genetically heterogenous disease with an immune-excluded microenvironment . NOTCH1 mutations were associated with worse, while MYB:NFIB fusion was not associated with prognosis . Our study shows that M2 macrophages and MYC are potential novel therapeutic targets in ACC.
TP53 (Tumor protein P53) • MYC (V-myc avian myelocytomatosis viral oncogene homolog) • NOTCH1 (Notch 1) • ARID1A (AT-rich interaction domain 1A) • KMT2C (Lysine Methyltransferase 2C) • KDM6A (Lysine Demethylase 6A) • MYB (MYB Proto-Oncogene, Transcription Factor) • EGF (Epidermal growth factor) • NFIB (Nuclear Factor I B)
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NOTCH1 mutation • MYC expression • NOTCH1 expression • MYB-NFIB fusion
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MI Tumor Seek™
6ms
The relative copy numbers of SOX-2 and NOTCH1 genetic loci was associated with increased expression of the epithelial-mesenchymal transition marker vimentin in tumor tissue samples and changed with each new generation of orthotopic xenografts.
Preclinical
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NOTCH1 (Notch 1) • SOX2 • VIM (Vimentin)
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NOTCH1 expression • VIM expression
6ms
We also provided preliminary data showing Notch as a therapeutic target of AB4. It would be interesting to investigate the anticancer efficacy of AB4 in other types of cancer with elevated Notch activity.
Journal
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NOTCH1 (Notch 1) • HES1
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NOTCH1 expression
6ms
Our analysis represents the largest real-world dataset of human SCLC tumors profiled by whole transcriptomic sequencing . The differential expression of immune genes and predictive biomarkers across SCLC subtypes may inform therapeutic vulnerabilities for rational and personalized treatment approaches in SCLC.
Real-world evidence • Clinical • Tumor Mutational Burden • MSi-H Biomarker
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EGFR (Epidermal growth factor receptor) • MYC (V-myc avian myelocytomatosis viral oncogene homolog) • NOTCH1 (Notch 1) • YAP1 (Yes associated protein 1) • SSTR2 (Somatostatin Receptor 2)
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EGFR mutation • MSI-H/dMMR • EGFR L858R • EGFR exon 19 deletion • MYC expression • NOTCH1 expression • SSTR2 expression
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MI Tumor Seek™
6ms
Combined, these results support selenite as a novel inhibitor of Notch signaling, and a plausible mechanism of inhibition has been proposed. This discovery highlights the potential value of selenite applied in a pathological context where Notch is a key drug target in diseases such as cancer, fibrosis, and neurodegenerative disorders.
Preclinical • Journal
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MYC (V-myc avian myelocytomatosis viral oncogene homolog) • NOTCH1 (Notch 1) • NOTCH2 (Notch 2) • HES1
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NOTCH1 expression
6ms
Previously, hesperetin, a citrus flavonoid, showed cytotoxicity in several cancer cells and increased cytotoxicity of doxorubicin and cisplatin. Taken together, hesperetin has potential for the treatment of BCSC by targeting p53, PPARG and Notch signaling. Further investigation of the molecular mechanisms involved is required for the development of hesperetin as a BCSC-targeted drug.
Preclinical • Journal
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TP53 (Tumor protein P53) • NOTCH1 (Notch 1) • PPARG (Peroxisome Proliferator Activated Receptor Gamma)
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TP53 expression • NOTCH1 expression
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cisplatin • doxorubicin hydrochloride
6ms
The strong immunoexpression of Notch1 can contribute to identification of patients with poorly differentiated oral squamous cell carcinoma, who have perineural infiltration or lymph node metastasis. In addition, the strong immunoexpression of ALDH1 may help to identify a worse prognosis in patients with oral squamous cell carcinoma and their subtypes.
Journal
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NOTCH1 (Notch 1) • ALDH1A1 (Aldehyde Dehydrogenase 1 Family Member A1)
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NOTCH1 expression
6ms
Our findings suggest that FXR represses Notch1 expression and directs ACD of Sox9 cells to prevent the development of liver cancer.
Preclinical • Journal
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NOTCH1 (Notch 1) • SOX9 (SRY-Box Transcription Factor 9)
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NOTCH1 expression • SOX9 expression • NOTCH1 overexpression
6ms
In summary, we for the first time provided evidence that TID could effectively inhibit osteosarcoma progression through repressing cell proliferation, inducing apoptosis, suppressing stem-cell-like properties via down-regulating AKT/GSK-3β/NOTCH1 signaling pathway. Thus, TID may be a promising therapeutic strategy for osteosarcoma treatment without side effects.
Journal
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NOTCH1 (Notch 1) • CASP3 (Caspase 3) • CDKN1A (Cyclin-dependent kinase inhibitor 1A)
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NOTCH1 expression
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Nypta (tideglusib)
6ms
Furthermore, TUG1 depletion inhibited the expression of Hes-1, Survivin, and Bcl-2 protein in MM cells and xenograft tumors. TUG1 knockdown inhibited MM tumorigenesis by regulating the miR-34a-5p/NOTCH1 signaling pathway in vitro and in vivo, deepening our understanding of the TUG1 function in MM.
Journal • IO biomarker
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BCL2 (B-cell CLL/lymphoma 2) • NOTCH1 (Notch 1) • BIRC5 (Baculoviral IAP repeat containing 5) • MIR34A (MicroRNA 34a-5p) • HES1
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BCL2 expression • BIRC5 expression • NOTCH1 expression
7ms
Our study revealed that the effect of miR mimic in target gene repression can be dependent to its concentration as well as to the cell type. Meanwhile, our findings further support a regulatory function for pre-miRNAs in target repression and will help to develop effective therapeutic strategies in cancer treatment.
Journal
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NOTCH1 (Notch 1) • CD44 • MIR34A (MicroRNA 34a-5p)
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NOTCH1 expression
7ms
Consequently, down-regulation of CRNDE could down-regulate tumour volume, simultaneously down-regulate the expression of CD163 and CD31 in tissues, decrease the expression of key proteins (including JAK-1, STAT-6, p-STAT6 and p-AKT1), and down-regulate the expression of key angiogenesis-related proteins (including VEGF, Notch1, Dll4 and VEGFR2). In this study, we found that CENDE could indirectly regulate tumour angiogenesis by promoting M2 polarization of macrophages, which is also one of the mechanisms of microenvironmental immune regulation in liver cancer.
Journal
|
NOTCH1 (Notch 1) • AKT1 (V-akt murine thymoma viral oncogene homolog 1) • KDR (Kinase insert domain receptor) • JAK1 (Janus Kinase 1) • CD163 (CD163 Molecule) • CCL2 (Chemokine (C-C motif) ligand 2) • TGFB1 (Transforming Growth Factor Beta 1) • CD31 (Platelet and endothelial cell adhesion molecule 1) • IL10 (Interleukin 10) • STAT6 (Signal transducer and activator of transcription 6) • CCL22 (C-C Motif Chemokine Ligand 22) • IL4 (Interleukin 4)
|
KDR expression • CD31 expression • NOTCH1 expression
7ms
In conclusion, NICD was upregulated in human GBM and NICD promoted GBM proliferation via the Notch1 signaling pathway. NICD may be a potential diagnostic marker and therapeutic target for GBM treatment.
Journal
|
NOTCH1 (Notch 1)
|
NOTCH1 expression
7ms
Overall, ANO induced initial stage carcinogenesis in the oral cavity via inflammation, ROS and depletion of antioxidant enzymes. Arecoline N-oxide mercapturic acid (NOM) attenuates the initiation of oral carcinogenesis.
Journal
|
NOTCH1 (Notch 1) • IL17A (Interleukin 17A) • IL1B (Interleukin 1, beta)
|
NOTCH1 expression
|
arecoline
7ms
Moreover, linc00641 sponged the expression of miR-429 and subsequently upregulated Notch-1 expression in gastric cancer cells. We concluded that linc00641 promoted the malignant progression of gastric cancer by modulating the miR-429/Notch-1 axis.
Journal
|
NOTCH1 (Notch 1) • MIR429 (MicroRNA 429)
|
NOTCH1 expression • miR-429 expression
7ms
Our data suggested that catalpol may promote OPC differentiation and remyelination through modulation of the NOTCH1 pathway. This study provides new insight into the mechanism of action of catalpol in the treatment of multiple sclerosis.
Journal
|
NOTCH1 (Notch 1) • HES1
|
NOTCH1 expression
7ms
In a previous study, we identified cell surface receptor, Trop2, as a novel driver of metastatic NEPC. Herein, our new findings reveal that Trop2 interacts with NOTCH1, SLC4A7, PLEC, and OCLN, which may highlight novel biological functions of Trop2 in prostate tumorigenesis and provide new understanding of the potential mechanism of neuroendocrine differentiation and metastasis to provide new therapeutic strategy for metastatic CRPC with neuroendocrine features.
NOTCH1 (Notch 1)
|
TROP2 overexpression • NOTCH1 expression • TROP2 expression
7ms
Collectively, these findings provide a strong molecular rationale for exploring PRT543 as a potential therapeutic option for ACC tumors. PRT543 is currently under evaluation in a Phase I clinical trial in patients with advanced solid tumors and hematological malignancies (NCT03886831).
NOTCH1 (Notch 1) • MYB (MYB Proto-Oncogene, Transcription Factor) • NFIB (Nuclear Factor I B) • PRMT5 (Protein Arginine Methyltransferase 5) • FOXM1 (Forkhead Box M1) • GATA3 (GATA binding protein 3) • SOX4 (SRY-Box Transcription Factor 4)
|
NOTCH1 mutation • NOTCH1 expression • MYB-NFIB fusion
|
PRT543
7ms
Combination of osimertinib and GSI delays proliferation of DT cells in EGFR mutated NSCLC by modulating Notch pathway.
EGFR (Epidermal growth factor receptor) • NOTCH1 (Notch 1) • HES1
|
EGFR mutation • EGFR T790M • EGFR H1975 • NOTCH1 expression
|
Tagrisso (osimertinib)
7ms
Furthermore, this approach models leukemic transformation and progression in vivo by allowing for crosstalk between leukemia cells and the microenvironment, an aspect unaccounted for in cell-line based in vitro studies. Thus, the HSC transduction and transplantation model more faithfully recapitulates development of the human disease, providing a highly comprehensive and versatile tool for further in vivo and ex vivo functional studies.
Journal
|
NOTCH1 (Notch 1)
|
NOTCH1 mutation • NOTCH1 expression
8ms
In turn, NOTCH1 downregulation induces resistant multicellular networks by TM extension. Our findings identify NOTCH1 as a central switch between the PVN and network niche in glioma, and demonstrate robust cross-compensation when only one niche is targeted.
Journal
|
NOTCH1 (Notch 1)
|
NOTCH1 expression
8ms
In this study, we aimed to determine whether HOXA-AS3 can mediate cisplatin resistance in bladder cancer, and its potential mechanism of action...Our findings indicate that HOXA-AS3 may function as a competing endogenous RNA (ceRNA) of miR-455-5p to regulate Notch1 and play an important role in regulating chemotherapeutic drug sensitivity in BC cells. Therefore, HOXA-AS3 may be a novel therapeutic target for treating bladder cancer.
Journal
|
NOTCH1 (Notch 1)
|
NOTCH1 expression
|
cisplatin
8ms
After modeling, the group treated with normal saline was taken as control group, 200 mg/kg of YQCTF was adopted for intervention, and the tumor volume and growth inhibition rate were compared with the vascular targeted inhibitor Sorafenib...YQCTF could inhibit the growth of lung cancer transplanted tumor through antiangiogenesis, and it could also reduce the amount of angiogenesis in lung cancer transplanted tumor. In addition, the generation of lumen structure was also hindered, which was realized through the VEGF signaling pathway and DLL4-Notch signaling pathway.
Journal
|
NOTCH1 (Notch 1) • HIF1A (Hypoxia inducible factor 1, alpha subunit) • CD31 (Platelet and endothelial cell adhesion molecule 1)
|
HIF1A expression • NOTCH1 expression • VEGFA expression
|
Nexavar (sorafenib)
8ms
Decrease in tumor cell survival following the exposure to ELF-MFs may be the result of decreased in the expression level of NOTCH1 and its Reg-circ-RNA. These magnetic field-reducing effects on cancer cell survival through the change on the expression of genes involved in the proliferation and progression of cancer can be a new key in cancer treatment.
Journal
|
NOTCH1 (Notch 1)
|
NOTCH1 expression
8ms
Collectively, the results indicated that miR-34b-5p functions as a tumor suppressor in RB via regulating the Notch signaling pathway. Therefore, miR-34b-5p may be explored for its utility as a therapeutic target in RB.
Journal
|
NOTCH1 (Notch 1) • RB1 (RB Transcriptional Corepressor 1) • NOTCH2 (Notch 2) • CD133 • SOX2 • NANOG (Nanog Homeobox)
|
NOTCH1 expression
8ms
Our pilot study has identified that high expression of the molecules linked with the NOTCH1 pathway is an important poor prognostic marker among childhood AML patients. NOTCH1 expression also shows cross-talk with several other signal transduction pathways especially TGF β / SETBP1 which are also linked with poor prognosis.
Clinical
|
FLT3 (Fms-related tyrosine kinase 3) • NOTCH1 (Notch 1) • SETBP1 (SET Binding Protein 1) • TGFB1 (Transforming Growth Factor Beta 1)
|
FLT3 mutation • NOTCH1 expression
8ms
Our results indicated that targeting of PIN1 serves as a promising therapeutic solution for the suppression of tumor progression processes in CRC.
Journal
|
NOTCH1 (Notch 1)
|
NOTCH1 expression
8ms
Moreover, SNHG3 inhibition or miR-139-5p mimic abolished the promotion of Notch1 overexpression on OVCAR3 proliferation and migration. In conclusion, SNHG3 could accelerate the proliferation and migration of OC cells by regulating miR-139-5p and Notch1.
Journal
|
NOTCH1 (Notch 1) • MIR139 (MicroRNA 139)
|
NOTCH1 expression • miR-139-5p expression • NOTCH1 overexpression
8ms
The significance of these novel findings reveals that the copolymer's intracellular activity is critically dependent on the size and structural shape. This report offers novel therapeutic insight into a dual mechanism of the FA-DABA-SMA copolymer for its therapeutic potential to treat cancer.
Journal
|
NOTCH1 (Notch 1) • CASP3 (Caspase 3) • HES1 • CASP7 (Caspase 7)
|
FOLR1 expression • NOTCH1 expression
8ms
Overexpression of Notch1 resisted the anti-tumor functions of CASK knockdown in pancreatic cancer cells. In conclusion, CASK knockdown suppressed the malignant behaviors of pancreatic cancer cells by inactivating the Notch pathway.
Journal
|
NOTCH1 (Notch 1)
|
NOTCH1 expression • NOTCH1 overexpression
8ms
Transfection of miR-133a mimic induced apoptosis and inhibited OSCC cell proliferation, migration, and invasion and this was demonstrated to be attributable to decreased CTBP2 expression and suppression of the Notch signaling pathway. Taken together, we concluded that miR-133a acted as a tumor suppressor in OSCC through inhibition of the Notch signaling pathway via binding to CTBP2.
Journal
|
NOTCH1 (Notch 1) • NOTCH3 (Notch Receptor 3) • HES1
|
NOTCH1 expression
8ms
Herein, we report an exophytic secondary breast angiosarcoma with MYC and NOTCH1 immunoreactivity. This case illustrates the utility of these markers for the identification of radiation-associated angiosarcoma with MYC and NOTCH1 expression, potential for targeted therapy and need to identify patients for further studies of the clinicopathologic and prognostic significance.
Journal
|
MYC (V-myc avian myelocytomatosis viral oncogene homolog) • NOTCH1 (Notch 1)
|
MYC expression • NOTCH1 expression
9ms
Journal
|
NOTCH1 (Notch 1)
|
NOTCH1 expression • NOTCH1 overexpression
9ms
Our findings suggest that abiraterone and docetaxel treatments affects the expression of Notch signal pathway proteins. But these drugs especially cause significant upregulation in Hes1 expression in PCa cells. Therefore, co-application of Notch signaling inhibitors together with docetaxel and abiraterone chemotherapy, it was thought that decreased Hes1 expression could be stopped the deterioration of the prognosis of the patient.
Journal
|
NOTCH1 (Notch 1) • HES1
|
NOTCH1 expression
|
docetaxel • abiraterone acetate
9ms
Finally, SACC collective invasion was increased via the Dll4/Notch1 signalling pathway in experiments that involved a stiff 3D gel, hypoxia and co‑culture with human endothelial cells. These findings indicated that the Dll4/Notch1 signalling pathway may be involved in the collective invasion of SACC, which may help to provide possible targets for the treatment of SACC.
Journal
|
NOTCH1 (Notch 1)
|
NOTCH1 expression • NOTCH1 overexpression
9ms
In NRL-PRL/Apc females, rapidly proliferating hyperplasias, characterized by β-catenin at cell junctions and high NOTCH1 expression, contrasted with slower growing lesions with nuclear β-catenin in Apc females. These studies demonstrate that PRL can powerfully modulate the incidence and phenotype of mammary tumors, shedding light on mechanisms whereby PRL elevates risk of breast cancer.
Journal
|
NOTCH1 (Notch 1)
|
NOTCH1 expression
9ms
Thus, the conclusive extermination of CSCs achieved that was associated with recurrence due to treatment failure. That can help to achieve a longer and better quality of life in a natural, economical way.
Preclinical • Journal
|
NOTCH1 (Notch 1) • CD44 • POU5F1 (POU Class 5 Homeobox 1)
|
NOTCH1 expression • EPCAM expression
9ms
Rub can inhibit the growth, migration and invasion of prostate cancer cell line DU145 and PC3. The mechanism may be related to the inhibition of Notch-1, MMP-2, MMP-9 and Hes-1 by Rub.
Journal
|
NOTCH1 (Notch 1) • HES1 • MMP2 (Matrix metallopeptidase 2) • MMP9 (Matrix metallopeptidase 9)
|
NOTCH1 expression
9ms
We functionally assessed the biological effects of the first-in-human tested blocking antibody against Notch1 receptor (brontictuzumab, BRON) in a collection of glioma stem-like cell (GSC) models and compared its effects to genetic Notch1 inhibition as well as classical pharmacological Notch inhibitor treatment using gamma-secretase inhibitor MRK003. We note that the observed phenotype seems only in part due to Notch1 blockage and the drug candidate leads to activation of off target signals. Further studies addressing a possible emergence of therapy resistance due to WNT activation need to be conducted. We further validated our 3D disease modeling technology to be of benefit for drug development projects.
Clinical • Journal
|
IDH1 (Isocitrate dehydrogenase (NADP(+)) 1) • NOTCH1 (Notch 1) • HES1
|
IDH1 mutation • NOTCH1 expression
|
MRK003 • brontictuzumab (OMP-52M51)
9ms
The decrease in the expression of Notch1 and AXIN2 preceded changes in the expression of all other genes, at 24 h of treatment in a dose-dependent manner, followed by the downregulation of most Wnt- and NOTCH-signaling genes. Collectively, we showed that not only Wnt but also NOTCH signaling is a primary target of suppression by SCD1 inhibition in CSCs, suggesting the possibility of targeting SCD1 against colon cancer in clinical settings.
Journal
|
NOTCH1 (Notch 1)
|
NOTCH1 expression
9ms
The apoptosis, proliferation, and susceptibility of K562/A02 cells to Adriamycin (ADR) were analyzed by flow cytometry and CCK8 assay, respectively...Moreover, inhibiting expression of HOTAIR could attenuate the expression of P21 and Notch1 and inhibit the phosphorylation of AKT in drug-resistant cells. In conclusion, our results demonstrated that LncRNA-HOTAIR is involved in MDR development of leukemia cells by regulating the expression of P21 and the AKT/Notch1 signaling pathway.
Journal
|
NOTCH1 (Notch 1) • HOTAIR (HOX Transcript Antisense RNA) • CDKN1A (Cyclin-dependent kinase inhibitor 1A)
|
NOTCH1 expression
|
doxorubicin hydrochloride
9ms
Collectively, ZFPM2-AS1 exerted an oncogenic role in cutaneous malignant melanoma progression via targeting miR-650/NOTCH1 signaling. Our study might offer a novel sight for cutaneous malignant melanoma treatment.
Journal
|
NOTCH1 (Notch 1)
|
NOTCH1 expression
10ms
For first-line treatment 80.8% of patients received cisplatin or carboplatin plus gemcitabine. The genomic profile of SCC encompasses important genes including TP53, PIK3CA and KEAP1. TP53 mutations could be associated with PDL1 expression, generating hypothesis regarding specific treatment options.
Journal • PD(L)-1 Biomarker • IO biomarker
|
PD-L1 (Programmed death ligand 1) • TP53 (Tumor protein P53) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • NOTCH1 (Notch 1) • KEAP1 (Kelch Like ECH Associated Protein 1) • KMT2D (Lysine Methyltransferase 2D) • MLL2 (Myeloid/lymphoid or mixed-lineage leukemia 2)
|
PD-L1 expression • TP53 mutation • PD-L1 overexpression • PIK3CA mutation • KEAP1 mutation • KMT2D mutation • NOTCH1 expression
|
PD-L1 IHC 22C3 pharmDx
|
cisplatin • carboplatin • gemcitabine • GEN-1
10ms
Finally, targeting Notch1 effectively suppressed TRPM7-induced growth and proliferation of glioma cells through cell G1/S arrest and apoptotic induction. TRPM7 is responsible for sustained Notch1 signaling activation, enhanced expression of GSC markers CD133 and ALDH1, and regulation of glioma stemness, which contributes to malignant glioma cell growth and invasion.
Journal
|
NOTCH1 (Notch 1) • CD133 • STAT3 (Signal Transducer And Activator Of Transcription 3) • ALDH1A1 (Aldehyde Dehydrogenase 1 Family Member A1)
|
NOTCH1 expression • CD133 expression
10ms
An appropriate amount of anti-angiogenic agents can reconstruct tumor blood vessels in a short period of time and form vascular homeostasis, increase the function of blood vessel perfusion and reverse the multidrug resistance of chemotherapy, which is also called "vascular normalization." Endostar (a recombinant human endostatin) was developed by China and as a multi-target anti-angiogenesis agent...In this study, the patients with cervical cancer within stage IIB2 were selected, endostar combined with cisplatin+paclitaxel neoadjuvant chemotherapy (NACT) before radical surgical operation was adopted, patients outcome and adverse reaction were followed up...Endostar restored vascular homeostasis in cervical cancer temporarily, enhanced chemotherapeutic agents effects in cervical cancer, increased patient OS ratio. Endostar+NACT treatment may provide a new target therapy for cervical cancer.
Clinical • Journal
|
NOTCH1 (Notch 1) • KDR (Kinase insert domain receptor) • CD31 (Platelet and endothelial cell adhesion molecule 1) • NOTCH4 (Notch 4)
|
KDR expression • NOTCH1 expression
|
cisplatin • paclitaxel • Endostar (recombinant human endostatin)
10ms
To sum up, these results proposed that XIST functioned as an endogenous sponge in promoting PC cell proliferation through competing for miR-137 to regulate Notch1 expression, and may provide more therapeutic targets for the patients with PC.
Journal
|
NOTCH1 (Notch 1)
|
NOTCH1 expression • NOTCH1 overexpression
10ms
Moreover, lower expression of Notch1 was related to distant metastasis in GC patients with a borderline statistical significance (p = 0.0549). These data may advance our understanding of the molecular biology that drives GC as well as provide potential targets for defining novel therapeutic strategies for GC treatment.
Journal
|
NOTCH1 (Notch 1) • MIR34A (MicroRNA 34a-5p) • CDX-2 • MIR93 (MicroRNA 93)
|
NOTCH1 expression
10ms
Compared with the blank control group, the protein expression of Notch1 and Dll4 decreased significantly in each concentration Res group, but the decrease of protein expression of Jagged1 and Hes-5 was not significant. In conclusion, Res regulates mRNA and protein expression of Notch1, Dll4 of MDA-MB-231 cells via Notch pathway.
Preclinical • Journal
|
NOTCH1 (Notch 1)
|
NOTCH1 expression
10ms
The study included 46 patients, with 21 and 25 of the patients having "sensitive" and "refractory" disease, respectively. The majority of patients had a high DLL3 expression (n = 38), while a minority had Notch 1-high expression (n = 10). The chi-square test showed that there was a statistically significant negative association between Notch1 and Ascl1 expression (p = 0.013). The overall survival for patients with Notch1- high vs. low expression was 8.1 vs. 12.4 months, respectively (p = 0.036). Notch1 expression was an independent prognostic factor in the multivariate analysis (p = 0.02). No other biomarker showed any prognostic impact in this highly selected SCLC cohort. DLL3 is highly expressed in the majority of advanced staged SCLC cases, as expected. In the same patient population, Notch1 expression might have a potential prognostic implication, by driving a non-neuroendocrine differentiation process. Given the small number of cases with Notch1 high expression, the results of this study needs to be confirmed on a larger cohort.
Clinical • Journal
|
NOTCH1 (Notch 1) • DLL3 (Delta Like Canonical Notch Ligand 3) • HES1
|
DLL3 expression • NOTCH1 expression
10ms
Flow cytometry demonstrated that miR‑34c‑5p inhibited the proliferation of HeLa cells while accelerating apoptosis. The present study concluded that miR‑34c‑5p was a tumor suppressor in CC and may be a novel measure for the future treatment of CC.
Journal
|
NOTCH1 (Notch 1)
|
NOTCH1 expression
10ms
CCN3 expression levels are correlated to markers of cell cycle arrest oppositely in PE and AIP by activating the FAK/AKT pathway in AIP or down-regulating in PE. This may be one mechanism to explain the different pathological features of placental diseases, PE and AIP.
Journal
|
NOTCH1 (Notch 1) • CCND1 (Cyclin D1) • CCNE1 (Cyclin E1) • CDKN1A (Cyclin-dependent kinase inhibitor 1A)
|
CCND1 expression • NOTCH1 expression
10ms
In addition, we observed that MCF7-TR cells were resistant to doxorubicin but not the MCF-7 cells. In the present study, we conclude that the treatment with tamoxifen induces multiple epigenetic alterations that lead to the development of MDR and stem-like phenotypes in breast cancers. Therefore, our study provides better insights to develop novel treatment regime to control the progression of breast cancer.
Journal
|
NOTCH1 (Notch 1) • CCND1 (Cyclin D1)
|
CCND1 expression • NOTCH1 expression
|
tamoxifen • doxorubicin hydrochloride
11ms
Furthermore, low NOS2 expression was significantly associated with a higher metastasis-free survival in ER breast cancer patients treated with tamoxifen. In conclusion, our data support that NO-targeted therapy in ER breast cancer may contribute to increase the efficacy of antihormonal therapy avoiding the development of resistance to these treatments.
Clinical • Journal
|
ER (Estrogen receptor) • NOTCH1 (Notch 1)
|
ER positive • NOTCH1 expression
|
tamoxifen
11ms
Functional rescue experiment suggested that miR-515-5p regulated RB cell proliferation and drug sensitivity via inhibiting Notch1 expression. It could be concluded that overexpressed miR-515-5p suppressed proliferation and drug resistance of RB cells by targeting Notch1 expression, indicating that miR-515-5p might constitute a promising therapy target for RB.
Journal
|
NOTCH1 (Notch 1) • RB1 (RB Transcriptional Corepressor 1)
|
NOTCH1 expression
11ms
miR-27 upregulation promoted the formation of subcutaneous tumor in nude mice. Collectively, miR-27 elevated Notch1 expression by targeting NEDD4 and promoted the development of MM by inhibiting cell autophagy, which provides a new idea and basis for MM treatment.
Journal
|
NOTCH1 (Notch 1) • SDC1 (Syndecan 1)
|
NOTCH1 expression
11ms
This functional interaction in developing thymocytes was confirmed in vivo using a phf6-deficient zebrafish model that also displayed accelerated developmental kinetics upon reduced phf6 or notch1 activation. In summary, our work reveals that appropriate control of PHF6 expression is important for normal human hematopoiesis and provides clues towards the role of PHF6 in T-ALL development.
Journal
|
NOTCH1 (Notch 1)
|
NOTCH1 expression
11ms
In summary, stemness transformation of ovarian cancer cells can be activated by SNORA72 through the Notch1/c-Myc pathway. This study introduces a novel therapeutic strategy for improving the treatment efficiency of ovarian cancer.
Journal
|
MYC (V-myc avian myelocytomatosis viral oncogene homolog) • NOTCH1 (Notch 1) • CD133 • POU5F1 (POU Class 5 Homeobox 1)
|
MYC expression • NOTCH1 expression
11ms
Matrine could promote the differentiation of HOCs into hepatocytes by inhibiting the Notch signalling pathway and alleviate liver injury.
Journal
|
NOTCH1 (Notch 1) • HES1
|
NOTCH1 expression
11ms
To our knowledge, this study is the first to demonstrate that ranolazine protects against DCM-induced apoptosis by activating the NOTCH1/NRG1 signaling pathway. Moreover, our study identified new mechanisms involved in DCM.
Journal
|
NOTCH1 (Notch 1) • NRG1 (Neuregulin 1) • BAX (BCL2-associated X protein) • CASP3 (Caspase 3)
|
NOTCH1 expression
11ms
MRP1 and Notch1 signaling pathway were confirmed to participate in Trop2-induced drug resistance. CONCLUSIONS Our findings suggest that Trop2 promotes the resistance of gastric cancer to chemotherapy by activating the Notch1 pathway.
Journal
|
NOTCH1 (Notch 1)
|
NOTCH1 expression • TROP2 expression
11ms
Hence, the crosstalk between Smarcd1 and Notch1, which formed a feedback loop, was crucial in regulation of glioblastoma malignant phenotypes. Furthermore, targeting Smarcd1 could be a potential strategy for human glioblastoma treatment.
Journal
|
NOTCH1 (Notch 1) • HES1 • SMARCD1 (SWI/SNF Related, Matrix Associated, Actin Dependent Regulator Of Chromatin, Subfamily D, Member 1)
|
NOTCH1 expression
11ms
Secretory carcinoma, previously known as mammary analog secretory carcinoma, is distinguished by an ETV6-NTRK3 fusion that can both help differentiate it from its morphologically similar acinar cell carcinoma and make it susceptible to Trk inhibitors. In the present article, we discuss the molecular abnormalities, their impact on tumor biology, and therapeutic opportunities for the most common SGC subtypes and review published and ongoing clinical trials and future perspectives for this rare disease.
Review • Journal
|
HER-2 (Human epidermal growth factor receptor 2) • NTRK3 (Neurotrophic tyrosine kinase, receptor, type 3) • AR (Androgen receptor) • NOTCH1 (Notch 1) • ETV6 (ETS Variant Transcription Factor 6)
|
HER-2 overexpression • NTRK3 fusion • ETV6-NTRK3 fusion • NOTCH1 mutation • AR expression • NOTCH1 expression
11ms
CircPDK1 is aberrantly expressed in RCC and promotes the metastasis of RCC cells mainly through sponging miR-377-3P and reducing its negative regulation of NOTCH1. Thus, circPDK1 may act as a therapeutic target and biomarker for RCC.
Journal
|
NOTCH1 (Notch 1)
|
NOTCH1 expression
11ms
This study indicated that XJR could effectively inhibit HCC and might exert its antitumor effect through the miR-200b-3p/Notch1 axis. These findings provided new avenues for the use of XJR for prevention and treatment of HCC.
Journal
|
NOTCH1 (Notch 1) • MIR200B (MicroRNA 200b)
|
NOTCH1 expression • miR-200-b expression
11ms
Numerous approaches of Notch 1 inhibition possess potential benefits in the management of various clinical aspects of cancer. The application of different Notch 1 inhibition modalities faces many challenges.
Clinical • Journal
|
NOTCH1 (Notch 1)
|
NOTCH1 expression
11ms
Notch1 expression in conjunction with the low proliferative activity of cells and the absence of p53 (Y5) protein may suggest that the mechanism of apoptosis is preserved in tumor cells, which expands indications for medical treatment of prostate cancer.
Journal
|
TP53 (Tumor protein P53) • NOTCH1 (Notch 1)
|
TP53 expression • NOTCH1 expression
11ms
EP promoted migration and enrichment of astrocytes to demyelinated tissue and induced astrocytes to express neurotrophic CNTF and BDNF as well as translation factor nestin, Sox2, and β-catenin, which should contribute to astrocytes to differentiate of oligodendrogenesis. At the same time, EP promoted astrocytes to phagocytized myelin debris for removing the harmful substances of myelin regeneration.
Journal
|
NOTCH1 (Notch 1) • SOX2 • GFAP (Glial Fibrillary Acidic Protein)
|
NOTCH1 expression
11ms
The results of microstructural observation on tumor showed that M2-type TAMs infiltrated into tumor increased with increased expression of Th2-type cytokines, but M1-type TAMs reduced with reduced expression of Th1-type cytokines. According to our results, the Notch signal transduction pathway participates in tumor occurrence and growth with a negative role by maintaining Th1/Th2 balance.
Journal
|
NOTCH1 (Notch 1) • CSF2 (Colony stimulating factor 2)
|
NOTCH1 expression
11ms
Aiming to reverse the NOTCH1-controlled anti-apoptotic program and chemoresistance, we next tested the combination of Vincristine, Dexamethasone and L-Asparaginase (VXL) with IACS-010759. In summary, we demonstrated that targeting OxPhos with IACS-010759 in combination with chemotherapy facilitates eradication of chemoresistant NOTCH1-driven T-ALL through direct targeting of the key metabolic regulators of OxPhos conferred by mutant NOTCH1 in T-ALL. Clinical trials rewiring metabolism by incorporation of OxPhos-i to standard-of-care therapy in patients with NOTCH1-mutated T-ALL are warranted to improve patients’ outcomes.
MYC (V-myc avian myelocytomatosis viral oncogene homolog) • NOTCH1 (Notch 1) • AFF1 (AF4/FMR2 Family Member 1)
|
NOTCH1 mutation • MYC expression • NOTCH1 expression
|
vincristine • IACS-010759
11ms
Two PAK inhibitors, PF3758309 (PF) and FRAX597, were used to block PAK kinase activity pharmacologically...The synergistic effect between PAK inhibitor PF and doxorubicin was also observed (Figure 7)...Conclusions : PAK1 and PAK2 play certain roles in the occurrence and recurrence of T-LBL, and their potential as novel biomarkers deserves further exploring. Our results underscore the potential of PAK inhibitor as effective target therapy for T-LBL.
Clinical
|
NOTCH1 (Notch 1) • CCND1 (Cyclin D1) • PAK1 (p21 (RAC1) activated kinase 1)
|
NOTCH1 expression • MSLN positive
|
doxorubicin hydrochloride • FRAX597 • PF-3758309
11ms
The prognosis of MNKPL was not satisfactory even though HCT was performed. The development of new therapeutic approaches based on these genetic analyses is highly expected.
FLT3 (Fms-related tyrosine kinase 3) • NRAS (Neuroblastoma RAS viral oncogene homolog) • NOTCH1 (Notch 1) • KMT2D (Lysine Methyltransferase 2D) • CREBBP (CREB binding protein) • CARD11 (Caspase Recruitment Domain Family Member 11) • CD34 (CD34 molecule) • CD33 (CD33 Molecule) • CD7 (CD7 Molecule) • FANCI (FA Complementation Group I) • NCAM1 (Neural cell adhesion molecule 1) • BCL11B (BAF Chromatin Remodeling Complex Subunit BCL11B) • MSH4 (MutS Homolog 4) • RECQL4( RecQ Like Helicase 4)
|
NRAS G13 • NOTCH1 expression • FANCI mutation • RECQL4 mutation
11ms
Our study demonstrated distinct functional differences between AML and non-AML-MSC and direct AML-MSC interaction as an indispensable factor in influencing cell proliferation, leukemogenesis, and survival in mice. We further identified and confirmed the role of Notch signaling in AML-MSC interaction. Therapeutically, Dex abrogated AML-MSC interaction, decreasing AML cell viability, and leukemic mice survival.
NOTCH1 (Notch 1)
|
NOTCH1 expression
|
dexamethasone
12ms
These findings are confirmed by separately analyzing the CD20-dim and CD20-bright cell fractions from SF3B1-mutated cases as well as by DVL2 knock-out experiments in CLL-like cell models. Altogether, the clinical and biological features that characterize NOTCH1-mutated CLL may also be recapitulated in SF3B1-mutated CLL, contributing to explain the poor prognosis of this CLL subset and providing the rationale for expanding novel agents-based therapies to SF3B1-mutated CLL.
Journal
|
CD20 (Membrane Spanning 4-Domains A1) • NOTCH1 (Notch 1) • SF3B1 (Splicing Factor 3b Subunit 1)
|
NOTCH1 mutation • SF3B1 mutation • NOTCH1 expression
12ms
Overexpression of SEMA6B in FTC-133 cells presented the inverse results. These findings demonstrated that SEMA6B exerts a tumorigenic effect in thyroid carcinoma by activating Notch signaling pathway, which provide a possible biomarker for thyroid carcinoma.
Journal
|
NOTCH1 (Notch 1) • CCND1 (Cyclin D1) • HES1
|
CCND1 expression • NOTCH1 expression
12ms
Additionally, downregulation of Notch1 and survival signaling in ASR-treated tumors confirmed the in vitro results. In conclusion, ASR490 appears to be a potent agent that can inhibit Notch1 signaling in CRC.
Journal
|
NOTCH1 (Notch 1) • NOTCH2 (Notch 2) • CDH1 (Cadherin 1) • NOTCH3 (Notch Receptor 3)
|
NOTCH1 expression • NOTCH3 expression
12ms
There is a strong association between the expression of Notch1 protein and the expression of Hes1, c-Myc and Jagged2 proteins, which could aid in better understanding tumorigenesis in SCLC.
Journal
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MYC (V-myc avian myelocytomatosis viral oncogene homolog) • NOTCH1 (Notch 1) • HES1
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MYC expression • NOTCH1 expression
12ms
In summary, our data demonstrate that cancer-secreted ECM1 induces a NOTCH-mediated endothelial feedback promoting cancer progression by enhancing migration and invasion. Targeting this interaction may provide a novel possibility to improve cancer treatment.
Journal
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HER-2 (Human epidermal growth factor receptor 2) • NOTCH1 (Notch 1) • NOTCH3 (Notch Receptor 3)
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HER-2 overexpression • HER-2 expression • NOTCH1 expression • NOTCH3 expression
1year
At last, Notch-1 overexpression or miR-137 inhibition could restore the DSCAM-AS1 silencing-mediated repressive function on cell proliferation and migration. The above data suggested that, DSCAM-AS1 may contribute to CRC cell proliferation and migration by targeting miR-137/Notch-1 axis.
Journal
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NOTCH1 (Notch 1)
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NOTCH1 expression
1year
Our study reveals that TET1 expression is strongly correlated with CCA tumorigenesis and the possibility of targeting TET1 in CCA patients who have wild-type IDH1.
IDH1 (Isocitrate dehydrogenase (NADP(+)) 1) • NOTCH1 (Notch 1) • TET2 (Tet Methylcytosine Dioxygenase 2)
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IDH1 mutation • NOTCH1 expression
1year
Overexpression of NKX2-1 via cDNA transfection caused more than 2.8-fold increases in NOTCH3, HEY1, and FOXJ1 mRNA levels in the HBE cells cultured under consecutive hypoxia compared to the levels under normoxia. Taken together, our results show for the first time that consecutive hypoxia decreased expression of the co-regulated gene module NOTCH3/HEY1/CC10 and the ciliogenesis-inducing transcription factor gene FOXJ1 via NKX2-1 mRNA downregulation, while intermittent H/R increased expression of the co-regulated gene module BMP4/NOTCH1/MKI67/OCT4 and the predominant airway mucin gene MUC5AC via HIF1A mRNA upregulation.
Journal
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NOTCH1 (Notch 1) • HIF1A (Hypoxia inducible factor 1, alpha subunit) • NOTCH3 (Notch Receptor 3) • POU5F1 (POU Class 5 Homeobox 1) • MUC5AC (Mucin 5AC)
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HIF1A expression • NOTCH1 expression • MSLN positive • NOTCH3 expression
1year
Collectively, our results indicated that Notch1 and Akt might play vital roles in sorafenib resistance in HCC cells and VPA might overcome the drug resistance to enhance the sensitivity of HCC cells to sorafenib through suppressing Notch/Akt signaling pathway. VPA combined with sorafenib may provide a potential targeting therapeutic regimen for clinically to solve the problem of sorafenib resistance.
Journal
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NOTCH1 (Notch 1)
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NOTCH1 expression
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Nexavar (sorafenib)
1year
NEAT1 promotes the proliferation of T-ALL cells by sponging miR-146b-5p to upregulate the expression of NOTCH1. The results of this study provide new insight into the action mechanism of NEAT1 modulating T-ALL progression.
Journal
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NOTCH1 (Notch 1)
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NOTCH1 expression
1year
In initiated(CD44+/CD24−/ALDH1+) BCSC tumor xenografts ectopically expressingmiR-34a, FCE/Doxorubicin combined treatment showed a significant regression in tumor size by 62% after 72h compared to untreated controls orDoxorubicin alone. All in all, the aberrant expression of selected miRNAs, such as of miR-34a, might regulate a crosstalk with stemness characteristic markers, Notch-1and ALDH1, that are involved in the pathogenesis of breast cancer.
Clinical
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NOTCH1 (Notch 1) • CD44 • CD24 (CD24 Molecule) • MIR34A (MicroRNA 34a-5p) • ALDH1A1 (Aldehyde Dehydrogenase 1 Family Member A1) • MIR142 (MicroRNA 142)
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NOTCH1 expression
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doxorubicin hydrochloride