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BIOMARKER:

NOTCH1 overexpression

i
Other names: NOTCH1, TAN1
Entrez ID:
Related biomarkers:
Associations
Trials
11d
Cepharanthine-mediated endoplasmic reticulum stress inhibits Notch1 via binding GRP78 for suppressing hepatocellular carcinoma metastasis. (PubMed, Phytomedicine)
Taken together, the present study finds that Cep possesses excellent anti-metastasis of HCC, wherein the GRP78 could be directly bound and activated by Cep, leading to ER stress and Notch1 blockage. This study reveals for the first time the effect, critical target, and mechanism of the Cep-mediated anti-cancer effect, providing novel insights into the molecular target therapy by phytomedicine.
Journal
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NOTCH1 (Notch 1) • MMP2 (Matrix metallopeptidase 2) • TGFB1 (Transforming Growth Factor Beta 1) • HSPA5 (Heat Shock Protein Family A (Hsp70) Member 5) • MMP9 (Matrix metallopeptidase 9)
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NOTCH1 expression • NOTCH1 overexpression
17d
LncRNA MACC1-AS1 facilitates the cell growth of small cell lung cancer by sequestering miR-579-3p and mediating NOTCH1-pathway. (PubMed, Int J Biol Macromol)
Rescue assays indicated that repressed SCLC cell growth caused by MACC1-AS1 knockdown could be reserved by miR-579-3p repression or NOTCH1 overexpression. In brief, lncRNA MACC1-AS1 boosted SCLC cell growth via sequestering miR-579-3p and mediating NOTCH1-pathway.
Journal
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NOTCH1 (Notch 1) • MACC1 (MET Transcriptional Regulator MACC1) • MACC1-AS1 (MACC1 Antisense RNA 1)
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NOTCH1 expression • MACC1 overexpression • NOTCH1 overexpression
2ms
Journal
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NOTCH1 (Notch 1) • NOTCH3 (Notch Receptor 3) • KDM1A (Lysine Demethylase 1A) • HES1 (Hes Family BHLH Transcription Factor 1)
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KDM1A expression • NOTCH1 overexpression
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iadademstat (ORY-1001)
2ms
Role of Notch 1 signaling and glycolysis in the pathogenic mechanism of adenomyosis (PubMed, Nan Fang Yi Ke Da Xue Xue Bao)
The Notch1 signaling pathway participates in the pathogenesis of AM possibly by regulating the proliferation, migration, invasion and glycolysis of endometrial cells.
Journal
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NOTCH1 (Notch 1) • MUC16 (Mucin 16, Cell Surface Associated) • SLC2A1 (Solute Carrier Family 2 Member 1)
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NOTCH1 expression • NOTCH1 overexpression
7ms
GHITM regulates malignant phenotype and sensitivity to PD-1 blockade of renal cancer cells via Notch signalling. (PubMed, J Cell Mol Med)
Furthermore, we also showed that YY1 could decrease GHITM level via binding to its promoter. Taken together, our study revealed that GHITM was a promising therapeutic target for KIRC, which could modulate malignant phenotype and sensitivity to PD-1 blockade of renal cancer cells via Notch signalling pathway.
Journal • PD(L)-1 Biomarker • IO biomarker
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NOTCH1 (Notch 1) • YY1 (YY1 Transcription Factor)
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NOTCH1 overexpression
8ms
Impact of NOTCH1 expression in primary breast adenoid cystic carcinoma. (PubMed, J Clin Pathol)
Our study demonstrates that in patients with breast AdCC, overexpression of NOTCH1 ≥20% is associated with larger tumour size and aggressive clinical outcomes. Importantly, NOTCH1 inhibitors may have potential therapeutic effect in patients with breast AdCC.
Journal
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NOTCH1 (Notch 1) • NFIB (Nuclear Factor I B)
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NOTCH1 expression • MYB-NFIB fusion • NOTCH1 overexpression
9ms
Prox1 Suppresses Proliferation and Drug Resistance of Retinoblastoma Cells via Targeting Notch1. (PubMed, Curr Med Sci)
These data show that Prox1 decreased RB cell proliferation and drug resistance by targeting Notch1, implying that Prox1 could be a potential therapeutic target for RB.
Journal
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NOTCH1 (Notch 1)
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NOTCH1 expression • NOTCH1 overexpression
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vincristine
10ms
N6-methyladenosine reader YTHDF1 promotes stemness and therapeutic resistance in hepatocellular carcinoma by enhancing NOTCH1 expression. (PubMed, Cancer Res)
Lipid nanoparticles targeting YTHDF1 significantly enhanced the efficacy of lenvatinib and sorafenib in HCC in vivo. Taken together, YTHDF1 drives HCC stemness and drug resistance through a YTHDF1-m6A-NOTCH1 epitranscriptomic axis, and YTHDF1 is a potential therapeutic target for treating HCC.
Journal
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NOTCH1 (Notch 1) • YTHDF1 (YTH N6-Methyladenosine RNA Binding Protein 1)
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NOTCH1 expression • NOTCH1 overexpression
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sorafenib • Lenvima (lenvatinib)
11ms
Chaperonin containing TCP1 subunit 6A may activate Notch and Wnt pathways to facilitate the malignant behaviors and cancer stemness in oral squamous cell carcinoma. (PubMed, Cancer Biol Ther)
Importantly, it was shown that activation of the Wnt or Notch pathways attenuated the effect of CCT6A knockout on SCC-15 cell survival, invasion, and stemness. CCT6A may promote OSCC malignant behavior and stemness by activating the Wnt and Notch pathways.
Journal
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NOTCH1 (Notch 1) • SOX2
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CD133 expression • SOX2 expression • NOTCH1 overexpression
12ms
Forkhead Box M1 Regulates the Proliferation,Invasion,and Drug Resistance of Gastric Cancer Cells via circ_NOTCH1 (PubMed, Zhongguo Yi Xue Ke Xue Yuan Xue Bao)
Objective To investigate the impacts of forkhead box M1(FOXM1)on the proliferation,invasion,and drug resistance of gastric cancer cells by regulating the circular RNA circ_NOTCH1.Methods Western blotting and real-time quantitative PCR were performed to determine the expression of FOXM1 protein and circ_NOTCH1,respectively,in the gastric cancer tissue,para-carcinoma tissue,human normal gastric mucosa epithelial cell line GES-1 and gastric cancer cell lines MGC-803,HGC-27,and BGC-823.BGC-823 cells were classified into the following groups:control,short hairpin RNA FOXM1(sh-FOXM1)and negative control(sh-NC),small interfering RNA circ_NOTCH1(si-circ_NOTCH1)and negative control(si-NC),and sh-FOXM1+circ_NOTCH1 overexpression plasmid(sh-FOXM1+pcDNA-circ_NOTCH1)and sh-FOXM1+negative control(sh-FOXM1+pcDNA).CCK-8 assay and clone formation assay were employed to measure the cell proliferation,and Transwell assay to measure cell invasion.After treatment with 1.0 mg/L adriamycin for 48 h,the cell resistance in each group was analyzed.Western blotting was employed to determine the expression levels of FOXM1,proliferating cell nuclear antigen(PCNA),Bax,multi-drug resistance-associated protein 1(MRP1),and multi-drug resistance gene 1(MDR1).RNA pull-down and RNA immunoprecipitation were employed to examine the binding of circ_NOTCH1 to FOXM1 protein.Results Compared with those in the para-carcinoma tissue,the expression levels of FOXM1 protein and circ_NOTCH1 in the gastric cancer tissue were up-regulated(all P<0.001).Compared with GES-1 cells,MGC-803,HGC-27,and BGC-823 cells showed up-regulated expression levels of FOXM1 protein and circ_NOTCH1(all P<0.001).Compared with the control group and sh-NC group,the sh-FOXM1 group with down-regulated expression of FOXM1 protein and circ_NOTCH1 showed decreased optical density value,clone formation rate,cell invasion number,and cell viability,down-regulated expression of PCNA,MRP1,and MDR1,and up-regulated expression of Bax protein in BGC-823 cells(all P<0.001).Compared with the control group and the si-NC group,the si-circ_NOTCH1 group with down-regulated expression of circ_NOTCH1 showed decreased optical density value,clone formation rate,cell invasion number,and cell viability,down-regulated expression of PCNA,MRP1,and MDR1,and up-regulated expression of Bax protein in BGC-823 cells(all P<0.001).Compared with sh-FOXM1 group and sh-FOXM1+pcDNA group,the sh-FOXM1+pcDNA-circ_NOTCH1 group with up-regulated expression of circ_NOTCH1 showed increased optical density value,clone formation rate,cell invasion number,and cell viability,up-regulated expression of PCNA,MRP1,and MDR1,and down-regulated expression of Bax protein(all P<0.001).FOXM1 protein was able to interact with circ_NOTCH1.Conclusion Interference with FOXM1 may inhibit the proliferation,invasion,and drug resistance of gastric cancer cells by silencing circ_NOTCH1 expression.
Journal
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ABCB1 (ATP Binding Cassette Subfamily B Member 1) • BAX (BCL2-associated X protein) • FOXM1 (Forkhead Box M1) • PCNA (Proliferating cell nuclear antigen)
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BAX expression • NOTCH1 overexpression • PCNA expression
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doxorubicin hydrochloride
12ms
In Vivo Modeling of T-Cell Acute Lymphoblastic Leukemia Reveals Synergistic Oncogenic Pathways and Bcl11b Haploinsufficiency As a Potential Therapeutic Vulnerability (ASH 2023)
Using our resource, we identified Bcl11b as a strong and selective context-specific dependency in T-ALL. Although Bcl11b is a transcription factor, our results could serve as an starting point for novel therapies that interfere with Bcl11b function, such as molecular glue degraders or protein interaction inhibitors.
Preclinical
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PTEN (Phosphatase and tensin homolog) • CDKN2A (Cyclin Dependent Kinase Inhibitor 2A) • NOTCH1 (Notch 1) • CD8 (cluster of differentiation 8) • ETV6 (ETS Variant Transcription Factor 6) • IL2RA (Interleukin 2 receptor, alpha) • PIK3CD (Phosphatidylinositol-4 5-Bisphosphate 3-Kinase Catalytic Subunit Delta) • PHF6 (PHD Finger Protein 6) • LMO2 (LIM Domain Only 2) • BCL11B (BAF Chromatin Remodeling Complex Subunit BCL11B) • TLX1 (T Cell Leukemia Homeobox 1)
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PTEN mutation • CDKN2A deletion • NRAS G12 • NOTCH1 deletion • CD4 positive • NOTCH1 overexpression
1year
Vitamin D Inhibits Colorectal Cancer Cell Proliferation, Migration and Invasion via Downregulating the Notch1 Pathway. (PubMed, Cell Mol Biol (Noisy-le-grand))
In addition, we found that Notch1 overexpression could significantly reverse the inhibitory effect of vitamin D on SW480 cells. These results reveal novel insights into the mechanisms of vitamin D anticancer activity in CRC development and progression.
Journal
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NOTCH1 (Notch 1)
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NOTCH1 expression • NOTCH1 overexpression
1year
Notch signaling regulates a metabolic switch through inhibiting PGC-1α and mitochondrial biogenesis in dedifferentiated liposarcoma. (PubMed, Oncogene)
Similarly, overexpression of PGC-1α is sufficient to rescue mitochondria biogenesis, inhibit the growth and promote adipogenic differentiation of DDLPS cells. Together, these data demonstrate that Notch activation inhibits PGC-1α to suppress mitochondrial biogenesis and drive a metabolic switch in DDLPS.
Journal
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NOTCH1 (Notch 1) • MDM2 (E3 ubiquitin protein ligase) • NICD (NOTCH1 intracellular domain) • PPARGC1A (PPARG Coactivator 1 Alpha)
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NOTCH1 overexpression
over1year
Notch1 promotes resistance to cisplatin by up-regulating Ecto-5'-nucleotidase (CD73) in triple-negative breast cancer cells. (PubMed, Cell Death Discov)
Using chromatin immunoprecipitation and Dual-Luciferase assay it was identified that N1ICD directly bound the CD73 promoter and activated transcription. Taken together, these findings suggest CD73 as a direct downstream target of Notch1, providing an additional layer to the mechanisms underlying Notch1-mediated cisplatin resistance in TNBC.
Journal
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NOTCH1 (Notch 1) • NT5E (5'-Nucleotidase Ecto) • NICD (NOTCH1 intracellular domain)
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NOTCH1 expression • CD73 expression • NOTCH1 overexpression
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cisplatin
over1year
Baicalin Antagonizes Prostate Cancer Stemness via Inhibiting Notch1/NF-κB Signaling Pathway. (PubMed, Chin J Integr Med)
Mechanistically, baicalin exhibited a potential therapeutic effect on PCa via inhibiting the Notch1/NF-κB signaling pathway and its mediated cancer stemness.
Journal
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NOTCH1 (Notch 1) • CD44 (CD44 Molecule) • ALDH1A1 (Aldehyde Dehydrogenase 1 Family Member A1) • RELA (RELA Proto-Oncogene)
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CD44 expression • NOTCH1 expression • CD133 expression • NOTCH1 overexpression
over1year
Distinct oncogenic phenotypes in hematopoietic specific deletions of Trp53. (PubMed, Sci Rep)
Interestingly, marginal zone and diffuse large B-cell lymphomas had a unique gene expression signature characterized by activation of the PI3K pathway, compared with wild type marginal zone or follicular cells of the spleen. This study demonstrates lineage specific P53 deletion leading to distinct phenotypes secondary to unique gene expression programs set in motion.
Journal
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TP53 (Tumor protein P53) • NOTCH1 (Notch 1) • CD19 (CD19 Molecule) • VAV1 (Vav Guanine Nucleotide Exchange Factor 1)
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TP53 deletion • NOTCH1 overexpression
over1year
Abrogation of stemness in osteosarcoma by the mithramycin analog EC-8042 is mediated by its ability to inhibit NOTCH-1 signaling. (PubMed, Biomed Pharmacother)
Overall, these data highlight the relevant role that NOTCH1 signaling plays in mediating stemness in osteosarcoma. Moreover, we demonstrate that EC-8042 is powerful inhibitor of NOTCH signaling and that the anti-CSC activity of this mithramycin analog highly rely on its ability to repress this pathway.
Journal
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NOTCH1 (Notch 1) • HES1 (Hes Family BHLH Transcription Factor 1)
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NOTCH1 expression • NOTCH1 overexpression
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AIT-102
over1year
METTL3-mediated Hsa_circ_0000390 downregulation enhances the proliferation, migration, and invasion of colorectal cancer cells by increasing Notch1 expression. (PubMed, Hum Cell)
Additionally, METTL3 overexpression could accelerate the proliferation, cell migration, and invasion of CRC cells, which also was weakened by circ_0000390 overexpression in CRC cells in vitro and in vivo. This study suggested that circ_0000390 might be anti-tumor factor in CRC and METTL3/Notch1 might be a therapeutic targets for CRC.
Journal
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NOTCH1 (Notch 1) • METTL3 (Methyltransferase Like 3)
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NOTCH1 expression • NOTCH1 overexpression
2years
KIF2A participates in the progression of hepatocellular carcinoma and angiogenesis by interacting with Notch1. (PubMed, Exp Ther Med)
The suppressive effects of KIF2A knockdown on HCC cell proliferation, migration, invasion and in vitro angiogenesis were partially reversed by Notch1 overexpression. Overall, KIF2A may act as an oncogene in HCC via activation of the Notch1 signaling pathway.
Journal
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NOTCH1 (Notch 1)
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NOTCH1 expression • NOTCH1 overexpression
2years
Sustained Aurora kinase B expression confers resistance to PI3K inhibition in head and neck squamous carcinoma. (PubMed, Cancer Res)
These data define a novel pathway in which Aurora B upregulates AKT that subsequently increases PDK1 selectively in NOTCH1MUT cells to mediate HNSCC survival in response to PI3K inhibition. These findings may lead to an effective therapeutic approach for HNSCC with NOTCH1 mutations while sparing normal cells.
Journal
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NOTCH1 (Notch 1) • AURKB (Aurora Kinase B)
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NOTCH1 mutation • NOTCH1 expression • NOTCH1 overexpression
2years
Identifying key mutations of radioresponsive genes in esophageal squamous cell carcinoma. (PubMed, Front Immunol)
These results indicate the differences of the germline mutations and somatic mutations between the radiosensitive and radioresistence groups in ESCC and imply that NOTCH1 plays important roles in regulating the radiosensitivity of ESCC. The findings might provide the biomarkers and potential treatment targets for improving the sensitivity to radiotherapy in ESCC.
Journal • Tumor Mutational Burden • IO biomarker
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PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • TMB (Tumor Mutational Burden) • MSI (Microsatellite instability) • NOTCH1 (Notch 1) • CD8 (cluster of differentiation 8) • KDR (Kinase insert domain receptor) • STAT3 (Signal Transducer And Activator Of Transcription 3)
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NOTCH1 expression • NOTCH1 overexpression
2years
Screening of four key genes in esophageal carcinoma based on TCGA and GEO data and verification of anti-proliferative effect of LAPTM4B knockdown in esophageal carcinoma cells invitro. (PubMed, Arch Biochem Biophys)
Notch1 overexpression abrogated LAPTM4B knockdown-induced proliferation reduction in ESCA cells. In conclusion, LAPTM4B silencing inhibited proliferation in ESCA cells by inactivating the Notch pathway.
Preclinical • Journal • IO biomarker
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BCL2 (B-cell CLL/lymphoma 2) • NOTCH1 (Notch 1) • AURKA (Aurora kinase A) • HES1 (Hes Family BHLH Transcription Factor 1)
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NOTCH1 overexpression
2years
DNMT3A Regulates miR-149 DNA Methylation to Activate NOTCH1/Hedgehog Pathway to Promote the Development of Junctional Osteosarcoma. (PubMed, Biomed Res Int)
Subsequently, the experimental results showed that miR-149 could target negative regulation of NOTCH1, and further overexpression of NOTCH1 in cells with high miR-149 expression could promote the growth and metastasis of osteosarcoma cells in vitro. The methyltransferase DNMT3A suppresses miR-149 expression by promoting methylation modification of the miR-149 promoter, resulting in elevated expression levels of NOTCH1 in cells, therefore exacerbating activation of the Hedgehog signaling pathway and therefore exacerbating the development and progression of osteosarcoma.
Journal • Epigenetic controller
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DNMT3A (DNA methyltransferase 1) • NOTCH1 (Notch 1) • MIR149 (MicroRNA 149)
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NOTCH1 expression • NOTCH1 overexpression
over2years
GRWD1 affects the proliferation, apoptosis, invasion and migration of triple negative breast cancer through the Notch signaling pathway. (PubMed, Exp Ther Med)
However, Notch1 overexpression reversed the effect of GRWD1 knockdown on biological behaviors of TNBC cells. In conclusion, GRWD1 knockdown could suppress the proliferation, invasion and migration and promoted apoptosis of TNBC cells through inhibiting the Notch signaling pathway.
Journal
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HER-2 (Human epidermal growth factor receptor 2) • MYC (V-myc avian myelocytomatosis viral oncogene homolog) • NOTCH1 (Notch 1) • CCND1 (Cyclin D1) • NOTCH4 (Notch 4) • EGF (Epidermal growth factor) • HES1 (Hes Family BHLH Transcription Factor 1) • CDKN1A (Cyclin-dependent kinase inhibitor 1A)
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CCND1 expression • NOTCH1 expression • NOTCH1 overexpression
over2years
Clinical and pathological impact of neuroendocrine lineage-specific transcription factors in adenocarcinoma of the colon. (EACR 2022)
None of the genes was correlated with any specific genotype. Conclusion Our data show that: i) ADC-NED are associated with specific profiles of transcriptional regulation; ii) the expression of these genes is influenced by the tumor genotype; iii) the association of some of these genes with clinical and pathological features support their potential role as novel biomarkers.
Clinical
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BRAF (B-raf proto-oncogene) • NOTCH1 (Notch 1) • DLL3 (Delta Like Canonical Notch Ligand 3) • YAP1 (Yes associated protein 1) • MYCL (MYCL Proto-Oncogene BHLH Transcription Factor) • POU2F3 (POU Class 2 Homeobox 3) • SYP (Synaptophysin) • ASCL1 (Achaete-Scute Family BHLH Transcription Factor 1) • NEUROD1 (Neuronal Differentiation 1)
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BRAF mutation • NOTCH1 expression • YAP1 underexpression • POU2F3 expression • NOTCH1 overexpression
over2years
The Notch signaling cascade as a prognostic factor (GSS 2022)
Of the 194 tumors, 53.1% (n=103) had low and 46.9% (n=91) high NOTCH1 RNA expression. After five years, 97.9% (95% CI 95.0-≥99.9) of the patients with low NOTCH1 expression were recurrence-free (RFI), in the group with high NOTCH1 expression 88.6% (95% CI 81.94 -95.26). The 5-year OS probability was more favorable for patients with low NOTCH1 expression than with high expression (90.6% 95% CI 84.7-96.5 and 84.1% 95% CI 76.5- 91.7).
NOTCH1 (Notch 1) • NOTCH4 (Notch 4) • JAG1 (Jagged Canonical Notch Ligand 1)
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NOTCH1 expression • NOTCH1 overexpression
over2years
NOTCH expression variability and relapse of breast cancer in high-risk groups. (PubMed, Am J Med Sci)
NOTCH1 and NOTCH3 were found to be overexpressed mainly in ERN tumors. HER2 and TN groups, are related to higher relapse rates. Therefore, anti-NOTCH therapy could be justified and implemented in conventional treatments of BC high-risk groups.
Journal
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HER-2 (Human epidermal growth factor receptor 2) • ER (Estrogen receptor) • NOTCH1 (Notch 1) • NOTCH3 (Notch Receptor 3)
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HER-2 overexpression • NOTCH1 expression • NOTCH3 expression • NOTCH1 overexpression
over2years
Prognostic value of NOTCH1 and OCT4 in gastric carcinoma. (PubMed, Indian J Pathol Microbiol)
Overexpression of NOTCH1 and OCT4 correlated with poor response to chemotherapy (P = 0.013, P = 0.005, respectively) and worse clinical outcome. Combined detection of these proteins might disclose even better predictive value for shorter survival and resistance to chemotherapy.
Journal
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NOTCH1 (Notch 1) • POU5F1 (POU Class 5 Homeobox 1)
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POU5F1 expression • NOTCH1 overexpression
over2years
Aurora kinase B expression shields HNSCC from PI3K inhibition-induced apoptosis through downstream mediators AKT and PDK1 (AACR 2022)
To use a pharmacologic approach, we combined the pan-Aurora kinase inhibitor danusertib (0-2µM) with PI3K/mTOR inhibitor omipalisib (0-200nM) in 56 HNSCC cell lines for 72h and observed a substantial decrease in cell viability in >80% of NOTCH1WT and >90% of NOTCH1MUT HNSCC lines...Mice bearing NOTCH1MUT xenografts showed complete tumor regression when treated with a combination of pan-PI3K inhibitor Copanlisib and Aurora inhibitor Alisertib as compared to control groups...We identified AURKB as a central player governing the sensitivity to PI3K inhibitor-induced apoptosis in the context of NOTCH1 mutation status in HNSCC through its effects on AKT and PDK1. These novel findings may lead to the development of more robust therapeutic approach for NOTCH1 mutant squamous carcinoma as well as patients who develop acquired resistance to targeted therapies.
PARP Biomarker
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NOTCH1 (Notch 1) • AURKA (Aurora kinase A) • CASP3 (Caspase 3) • AURKB (Aurora Kinase B)
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NOTCH1 mutation • AURKB overexpression • NOTCH1 overexpression
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Aliqopa (copanlisib) • omipalisib (GSK2126458) • alisertib (MLN8237) • danusertib (PHA-739358)
over2years
Abnormal activation of notch 1 signaling causes apoptosis resistance in cervical cancer. (PubMed, Int J Clin Exp Pathol)
Further, the NOTCH1 depleted cells showed increased sensitivity towards DNA-targeting drugs and therefore cell viability was reduced efficiently. Altogether, our findings suggest that Notch1 overexpression in cervical cancer cells was involved in tumorigenesis and apoptosis resistance of cervical cancer.
Journal
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NOTCH1 (Notch 1)
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NOTCH1 expression • NOTCH1 overexpression
almost3years
LncRNA FENDRR Inhibits Gastric Cancer Cell Proliferation and Invasion via the miR-421/SIRT3/Notch-1 Axis. (PubMed, Cancer Manag Res)
Nude mice injected with FENDRR overexpressing AGS cells had smaller tumor volume and weight and weaker tumor cell proliferation ability. FENDRR inhibits Notch-1 pathway to inhibit GC cell proliferation and invasion by upregulating SIRT3 expression via targeting miR-421.
Journal
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NOTCH1 (Notch 1) • SIRT3 (Sirtuin 3)
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NOTCH1 expression • SIRT3 expression • NOTCH1 overexpression
almost3years
Circ_0000745 regulates NOTCH1-mediated cell proliferation and apoptosis in pediatric T-cell acute lymphoblastic leukemia through adsorbing miR-193b-3p. (PubMed, Hematology)
Importantly, circ_0000745 regulated NOTCH1 expression by sponging miR-193b-3p. Our findings proposed a novel model in which circ_0000745 promoted cell proliferation and curbed cell apoptosis via upregulating NOTCH1 through serving as a miR-193b-3p sponge in T-ALL.
Clinical • Journal
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NOTCH1 (Notch 1) • MIR193B (MicroRNA 193b)
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NOTCH1 expression • NOTCH1 overexpression
3years
Rutin Mediated Apoptotic Cell Death in Caski Cervical Cancer Cells via Notch-1 and Hes-1 Downregulation. (PubMed, Life (Basel))
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) • CASP9 (Caspase 9) • HES1 (Hes Family BHLH Transcription Factor 1)
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BCL2 expression • CCND1 expression • NOTCH1 expression • CCND1 expression + CDK4 expression • NOTCH1 overexpression
over3years
DLX5 promotes osteosarcoma progression via activation of the NOTCH signaling pathway. (PubMed, Am J Cancer Res)
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 (Hes Family BHLH Transcription Factor 1)
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MYC expression • NOTCH1 expression • NOTCH1 overexpression
over3years
YAP Accelerates NOTCH Driven Cholangiocarcinogenesis via mTORC1 in Mice. (PubMed, Am J Pathol)
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
over3years
Hypoxia Promotes Pancreatic Cancer Cell Dedifferentiation to Stem-Like Cell Phenotypes With High Tumorigenic Potential by the HIF-1α/Notch Signaling Pathway. (PubMed, Pancreas)
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 (CD44 Molecule) • NES (Nestin)
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NOTCH1 expression • HIF1A expression • NOTCH1 overexpression