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BIOMARKER:

AKT1 overexpression

i
Other names: AKT1, AKT, PKB, PRKBA, RAC, V-akt murine thymoma viral oncogene homolog 1
Entrez ID:
Related biomarkers:
15d
Chitinase 3 like-1 activates the Akt pathway, inducing NF-κB-dependent release of pro-inflammatory cytokines and promoting the proliferative ability in nasopharyngeal carcinoma cells. (PubMed, Cytokine)
CHI3L1 knockdown inhibited NF-κB-dependent inflammatory response and promoting proliferation in NPC cells by inactivating the Akt pathway.
Journal
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IL6 (Interleukin 6) • TNFA (Tumor Necrosis Factor-Alpha) • CHI3L1 (Chitinase 3-like 1)
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AKT1 overexpression • IL6 expression
27d
Isoglutaminyl Cyclase Overexpression Enhances KYSE30 Cancer Cell Proliferation and Migration via the MAPK Signaling Pathway. (PubMed, J Proteome Res)
These phenotypes were inhibited upon exposure to PER2 inhibitor KL044, which allowed for the restoration of p-ERK levels. These data support upregulated isoQC being able to promote cancer cell proliferation and migration in vitro, likely by helping to regulate the MAPK and RAS signaling pathways, and the circadian protein PER2 might be a potential mediator.
Journal
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MAPK1 (Mitogen-activated protein kinase 1) • PER2 (Period Circadian Regulator 2)
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AKT1 overexpression
2ms
Tyrosine-phosphorylated DNER sensitizes insulin signaling in hepatic gluconeogenesis by inducing proteasomal degradation of TRB3. (PubMed, Mol Metab)
Taken together, the crosstalk between insulin-Akt and DNER-TRB3 pathways represents a previously unrecognized mechanism by which insulin regulates hepatic gluconeogenesis.
Journal
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EGF (Epidermal growth factor)
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AKT1 overexpression
2ms
Caffeic acid phenethyl ester suppresses the expression of androgen receptor variant 7 via inhibition of CDK1 and AKT. (PubMed, Cancer Gene Ther)
Intraperitoneal injection of 10 mg/kg CAPE retarded the growth of 22Rv1 xenografts in nude mice and suppressed the protein levels of AR-V7, CDK1 and AKT in 22Rv1 xenografts. Our study provided the rationale of applying CAPE for inhibition of AR-V7 in prostate tumors.
Journal
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AR (Androgen receptor) • AKT1 (V-akt murine thymoma viral oncogene homolog 1) • CDK1 (Cyclin-dependent kinase 1)
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AR overexpression • AR expression • AR splice variant 7 • AR-V7 expression • AKT1 overexpression • AR-V7 overexpression • AR splice variant 7 expression • CDK1 overexpression
3ms
High levels of fatty acid-binding protein 5 excessively enhances fatty acid synthesis and proliferation of granulosa cells in polycystic ovary syndrome. (PubMed, J Ovarian Res)
FABP5 promotes active fatty acid synthesis and excessive proliferation of GCs by activating PI3K-AKT signaling, suggesting that abnormally high expression of FABP5 in GCs may be a novel biomarker or a research target for PCOS treatment.
Journal
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AKT1 (V-akt murine thymoma viral oncogene homolog 1) • PCNA (Proliferating cell nuclear antigen) • FABP5 (Fatty Acid Binding Protein 5)
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AKT1 overexpression • PCNA expression
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LY294002
4ms
Insulin-like growth factor 2 mRNA-binding protein 3 enhanced melanoma migration through regulation of AKT1 and RELA expression. (PubMed, Exp Dermatol)
Human melanoma samples with high IMP-3 levels also showed high HMGA2, AKT1 and RELA expression. Our results show that IMP-3 enhances melanoma cell migration through the regulation of the AKT1 and RELA axis.
Journal
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RB1 (RB Transcriptional Corepressor 1) • AKT1 (V-akt murine thymoma viral oncogene homolog 1) • HMGA2 (High mobility group AT-hook 2) • IGF2BP3 (Insulin Like Growth Factor 2 MRNA Binding Protein 3) • MAPK3 (Mitogen-Activated Protein Kinase 3) • RELA (RELA Proto-Oncogene)
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AKT1 overexpression • HMGA2 expression • RELA expression
4ms
Molecular Mechanism Analysis of the Effect of Hederagenin Combined with L-OHP on Chemosensitivity of AGS/L-OHP Based on Network Pharmacology. (PubMed, Curr Comput Aided Drug Des)
Our findings suggest that HD may reduce the resistance of AGS/L-OHP cells to LOHP by regulating the PI3K/Akt signaling pathway.
Journal • IO biomarker
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BCL2 (B-cell CLL/lymphoma 2) • BIRC5 (Baculoviral IAP repeat containing 5)
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BCL2 expression • AKT1 overexpression • BIRC5 expression
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oxaliplatin
4ms
Discovery of novel Akt1 inhibitors by an ensemble-based virtual screening method, molecular dynamics simulation, and in vitro biological activity testing. (PubMed, Mol Divers)
The average binding free energies for the Akt1-CQU, Akt1-Ipatasertib, and Akt1-Hit9 systems were - 34.44, - 63.37, and - 39.14 kJ mol, respectively. In summary, the results obtained in this investigation suggested that Hit9 with novel scaffold may be a promising lead compound for developing new Akt1 inhibitor for treatment of various cancers with Akt1 overexpressed.
Preclinical • Journal
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AKT1 (V-akt murine thymoma viral oncogene homolog 1)
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AKT1 overexpression
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ipatasertib (RG7440)
4ms
Use of antioxidant nanoliposomes for co-delivery of PTEN plasmids and plumbagin to induce apoptosis in hepatic cancer cells. (PubMed, Biomed Mater)
Other cellular events such as Caspase-7 overexpression and PI3K, AKT, PARP, and mTOR inhibition led to the apoptosis in hepatic cancer cells. The mRNA expression profile of PTEN, PI3K, AKT3, caspase-7, PARP and mTOR proteins, primarily controlling the cancer cell proliferation and apoptosis, suggest that exogenous supply of PTEN could regulate the expression of oncogenic proteins and thus cancer progression.
Journal • PARP Biomarker
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PTEN (Phosphatase and tensin homolog) • CASP7 (Caspase 7)
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PTEN mutation • PTEN expression • AKT1 overexpression • PARP1 overexpression
4ms
CLEC19A overexpression inhibits tumor cell proliferation/migration and promotes apoptosis concomitant suppression of PI3K/AKT/NF-κB signaling pathway in glioblastoma multiforme. (PubMed, BMC Cancer)
To our knowledge, this is the first report providing in-silico, molecular, cellular, and in vivo evidences on the role of CLEC19A as a putative tumor suppressor gene in GBM. These results enhance our understanding of the role of CLEC19A in glioma and warrant further exploration of CLEC19A as a potential therapeutic target for GBM.
Journal • Tumor cell
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PTEN (Phosphatase and tensin homolog) • AKT1 (V-akt murine thymoma viral oncogene homolog 1) • MMP2 (Matrix metallopeptidase 2) • TIMP3 (TIMP Metallopeptidase Inhibitor 3)
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AKT1 overexpression
6ms
The key cellular senescence related molecule RRM2 regulates prostate cancer progression and resistance to docetaxel treatment. (PubMed, Cell Biosci)
Our findings suggest that RRM2 regulates docetaxel resistance in prostate cancer by stabilizing ANXA1-mediated activation of the PI3K/AKT pathway. Targeting RRM2 or ANXA1 may offer a promising therapeutic strategy to overcome docetaxel resistance in prostate cancer.
Journal
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ANXA1 (Annexin A1) • RRM2 (Ribonucleotide Reductase Regulatory Subunit M2)
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AKT1 overexpression • ANXA1 overexpression • ANXA1 expression
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docetaxel • COH29
6ms
New emerging targets in osteosarcoma therapy: PTEN and PI3K/Akt crosstalk in carcinogenesis. (PubMed, Pathol Res Pract)
Silencing PI3K/Akt by compounds and drugs can suppress OS. Here, we review in detail the function of the PTEN/PI3K/Akt in OS, revealing its biological function, function in tumor progression, resistance to therapy, and pharmacological significance.
Review • Journal
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PTEN (Phosphatase and tensin homolog) • AKT1 (V-akt murine thymoma viral oncogene homolog 1)
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PTEN mutation • PTEN expression • AKT1 overexpression
7ms
KIRREL promotes the proliferation of gastric cancer cells and angiogenesis through the PI3K/AKT/mTOR pathway. (PubMed, J Cell Mol Med)
IGF-1, an AKT agonist, and LY294002, an inhibitor, reversed the effects of KIRREL silencing and overexpression on the PI3K/AKT/mTOR pathway and on gastric cancer cell proliferation and angiogenesis. KIRREL may mediate the proliferation and angiogenesis of gastric cancer cells through the PI3K/AKT/mTOR signalling pathway. These findings could help in the further development of potential anti-angiogenesis targets.
Journal
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HIF1A (Hypoxia inducible factor 1, alpha subunit) • IGF1 (Insulin-like growth factor 1)
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AKT1 overexpression • HIF1A expression
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LY294002
7ms
CIP2A interacts with AKT1 to promote the malignant biological behaviors of oral squamous cell carcinoma by upregulating the GSK‑3β/β‑catenin pathway. (PubMed, Exp Ther Med)
In conclusion, CIP2A could interact with AKT1 to promote the malignant biological behaviors of OSCC cells by upregulating the GSK-3β/β-catenin pathway. These findings may provide a targeted therapy for OSCC treatment.
Journal
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AKT1 (V-akt murine thymoma viral oncogene homolog 1) • CIP2A (Cellular Inhibitor Of PP2A)
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AKT1 overexpression • CIP2A elevation • CDC42 elevation
9ms
Ginsenoside Rg3 inhibits the malignant progression of cervical cancer cell by regulating AKT2 expression. (PubMed, Heliyon)
Moreover, ginsenoside Rg3 treatment partially reversed AKT2 overexpression-mediated reduction in cell proliferation, migration, invasion, and tube formation. In conclusion, the above findings suggested that ginsenoside Rg3 inhibits CC progression via regulation of AKT2 expression, which might provide a potential therapeutic target for tumor therapy.
Journal
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AKT1 (V-akt murine thymoma viral oncogene homolog 1) • AKT2 (V-akt murine thymoma viral oncogene homolog 2)
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AKT1 overexpression • AKT2 expression
11ms
Serine protease PRSS56, a novel cancer-testis antigen activated by DNA hypomethylation, promotes colorectal and gastric cancer progression via PI3K/AKT axis. (PubMed, Cell Biosci)
Serine protease PRSS56 is a novel CT antigen that is reactivated in cancers by promoter DNA hypomethylation. PRSS56 functions oncogenic roles in GC and CRC by activating of PI3K/AKT axis. Our results presented here represent the first data on the function of the serine protease PRSS56 in cancers.
Journal • IO biomarker
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AKT1 (V-akt murine thymoma viral oncogene homolog 1)
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AKT1 overexpression
11ms
AKT inhibition interferes with the expression of immune checkpoint proteins and increases NK-induced killing of HL60-AML cells. (PubMed, Einstein (Sao Paulo))
The AKT pathway is involved in resistance to natural Killer-induced apoptosis in HL60 cells by regulating the expression of immune suppressor receptors. These findings highlight the importance of AKT in contributing to immune evasion mechanisms in acute myeloid leukemia and suggests the potential of AKT inhibition as an adjunct to immunotherapy.
Journal • PD(L)-1 Biomarker • IO biomarker
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PD-L1 (Programmed death ligand 1) • PD-1 (Programmed cell death 1) • HAVCR2 (Hepatitis A Virus Cellular Receptor 2) • TNFRSF1A (TNF Receptor Superfamily Member 1A) • CD96 (CD96 Molecule) • LGALS9 (Galectin 9)
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PD-1 expression • HAVCR2 expression • AKT1 overexpression
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perifosine (D21266)
11ms
The MyD88 inhibitor, ST2825, induces cell cycle arrest and apoptosis by suppressing the activation of the NF‑κB/AKT1/p21 pathway in pancreatic cancer. (PubMed, Oncol Rep)
MyD88 may thus serve as a potential therapeutic target in PDAC. ST2825 may serve as a novel agent for the targeted therapy of PDAC in the future.
Journal
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MYD88 (MYD88 Innate Immune Signal Transduction Adaptor)
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AKT1 overexpression
12ms
The effect of quercetin in the yishen tongluo jiedu recipe on the development of prostate cancer through the akt1-related CXCL12/CXCR4 pathway. (PubMed, Comb Chem High Throughput Screen)
As the active component of the Yishen Tongluo Jiedu recipe, quercetin inhibited PCa development through the Akt1-related CXCL12/CXCR4 pathway. This study provided a new idea for PCa treatment and a theoretical basis for further research.
Journal • IO biomarker
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BCL2 (B-cell CLL/lymphoma 2) • AKT1 (V-akt murine thymoma viral oncogene homolog 1) • CXCR4 (Chemokine (C-X-C motif) receptor 4) • CXCL12 (C-X-C Motif Chemokine Ligand 12) • CASP3 (Caspase 3)
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BCL2 expression • AKT1 overexpression • CXCL12 expression • CXCR4 expression
12ms
PLEKHG5 is stabilized by HDAC2-related deacetylation and confers sorafenib resistance in hepatocellular carcinoma. (PubMed, Cell Death Discov)
Our work showed a novel mechanism: HDAC2-mediated PLEKHG5 posttranslational modification maintains sorafenib resistance. This is a proof-of-concept study on targeting HDAC2 and PLEKHG5 in sorafenib-treated HCC patients as a new pharmaceutical intervention for advanced HCC.
Journal
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AKT1 (V-akt murine thymoma viral oncogene homolog 1) • HDAC2 (Histone deacetylase 2)
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AKT1 overexpression
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sorafenib
1year
CTSG Suppresses Colorectal Cancer Progression through Negative Regulation of Akt/mTOR/Bcl2 Signaling Pathway. (PubMed, Int J Biol Sci)
Furthermore, the Akt suppression signaling pathway by MK2206 abolishes CTSG-silenced expression-induced cell viability and Bcl2 up-regulation in vitro and in vivo. Altogether, these outcomes demonstrate that CTSG may act as a tumor suppressor gene via Akt/mTOR/Bcl2-mediated anti-apoptotic signaling inactivation, and CTSG represents a potential therapeutic target in CRC.
Journal • IO biomarker
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BCL2 (B-cell CLL/lymphoma 2) • CTSG (Cathepsin G)
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BCL2 expression • AKT1 overexpression
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MK-2206
1year
An Immunohistochemical Study of Breast Cancer Brain Metastases: The Role of CD44 and AKT in the Prognosis. (PubMed, Appl Immunohistochem Mol Morphol)
Immunohistochemistry markers such as CD44 and AKT may have a prognostic impact on survival in patients with breast cancer brain metastases. The conjugation with other markers may help with the stratification of patients and therapy.
Retrospective data • Journal • PD(L)-1 Biomarker • IO biomarker
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HER-2 (Human epidermal growth factor receptor 2) • PD-L1 (Programmed death ligand 1) • PTEN (Phosphatase and tensin homolog) • AKT1 (V-akt murine thymoma viral oncogene homolog 1) • CD44 (CD44 Molecule) • CA9 (Carbonic anhydrase 9) • ALDH1A1 (Aldehyde Dehydrogenase 1 Family Member A1) • PI3K (Phosphoinositide 3-kinases)
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HER-2 expression • AKT1 overexpression • CD44 expression • CA9 expression
1year
COPS6 promotes tumor progression and reduces CD8 T cell infiltration by repressing IL-6 production to facilitate tumor immune evasion in breast cancer. (PubMed, Acta Pharmacol Sin)
We conclude that COPS6 promotes breast cancer progression by reducing CD8 T cell infiltration and function via the regulation of IL-6 secretion. This study clarifies the role of p53/COPS6/IL-6/CD8 tumor infiltrating lymphocytes signaling in breast cancer progression and immune evasion, opening a new path for development of COPS6-targeting therapies to enhance tumor immunogenicity and treat immunologically "cold" breast cancer.
Journal • IO biomarker
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CD8 (cluster of differentiation 8) • IL6 (Interleukin 6)
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AKT1 overexpression
1year
Carboxypeptidase A6 suppresses the proliferation and invasion of colorectal cancer cells and is negatively regulated by miR-96-3p. (PubMed, Arch Biochem Biophys)
CPA6 has a significant tumor suppressive effect on CRC by inhibiting the activation of Akt/mTOR signaling, and miR-96-3p negatively regulates the expression of CPA6.
Journal
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MIR96 (MicroRNA 96) • CPA6 (Carboxypeptidase A6)
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AKT1 overexpression
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MK-2206
1year
Xihuang Pill-destabilized CD133/EGFR/Akt/mTOR cascade reduces stemness enrichment of glioblastoma via the down-regulation of SOX2. (PubMed, Phytomedicine)
We demonstrate for the first time that XHP down-regulates stemness, restrains self-renewal and induces apoptosis in GSCs and impedes glioma growth by down-regulating SOX2 through destabilizing the CD133/EGFR/Akt/mTOR cascade.
Journal
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EGFR (Epidermal growth factor receptor) • SOX2
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AKT1 overexpression • CD133 expression • CD133 positive • SOX2 expression
1year
IGFBP‑rP1 affects the proliferation, apoptosis and macrophage polarization of endometrial cancer cells by regulating the PI3K/AKT pathway. (PubMed, Exp Ther Med)
Overexpression of AKT in EC cells abolished the inhibitory effect of IGFBP-rP1 on M2 polarization. IGFBP-rP1 as an oncogenic factor inhibits M2 polarization of TAMs through PI3K/AKT signaling pathway and may be a potentially valuable target for EC therapy.
Journal
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AKT1 (V-akt murine thymoma viral oncogene homolog 1) • IGFBP7 (Insulin Like Growth Factor Binding Protein 7)
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AKT1 overexpression • IGFBP7 overexpression
1year
KAT7 promotes radioresistance through upregulating PI3K/AKT signaling in breast cancer. (PubMed, J Radiat Res)
Moreover, overexpression of KAT7, but not KAT7 acetyltransferase activity-deficient mutants promoted AKT phosphorylation at the Ser473 site, PIK3CA expression and radioresistance suppression due to KAT7 inhibition. In conclusion, KAT7 has huge prospects for clinical application as a new target for predicting radioresistance in breast cancer patients.
Journal
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PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • AKT1 (V-akt murine thymoma viral oncogene homolog 1)
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PIK3CA mutation • AKT1 overexpression • PIK3CA expression • PIK3CA overexpression
1year
Synergistic efficacy of telomerase-specific oncolytic adenoviral therapy and histone deacetylase inhibition in human hepatocellular carcinoma (AACR 2023)
MK-2206 was used to inhibit the activation of Akt signaling. Combination therapy with Telomelysin and AR42 demonstrates synergistic anti-HCC efficacy. Clinical trials investigating this new combination regimen are warranted.Keywords: Hepatocellular carcinoma, oncolytic adenovirus, Telomelysin, HDAC inhibitor, Akt
Clinical • Oncolytic virus • Epigenetic controller
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TERT (Telomerase Reverse Transcriptase)
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AKT1 overexpression
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MK-2206 • Telomelysin (suratadenoturev)
over1year
IHC expression of AKT in different grades of epithelial dysplasia: An in vitro study. (PubMed, J Oral Maxillofac Pathol)
An overall significant difference was observed when normal tissues were compared with epithelial dysplasia with a Chi-square value of 21.04, but there was no statistical significance between the three grades of epithelial dysplasias. In conclusion, this study suggests that Akt-1 overexpression can be one of the useful diagnostic markers for predicting the potential behaviour of oral dysplasias transforming into oral squamous cell carcinoma (OSCC).
Preclinical • Journal
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AKT1 (V-akt murine thymoma viral oncogene homolog 1)
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AKT1 overexpression
over1year
Co-encapsulation of PI3-Kδ/HDAC6 dual inhibitor and Navitoclax in Quatramer™ nanoparticles for synergistic effect in ER+ breast cancer. (PubMed, Int J Pharm)
The PI3-Kδ/HDAC6-NAV-NPs treatment (4 mg/kg, I.V., twice a week for three weeks) of ER breast cancer syngeneic mice tumor model resulted in complete tumor eradication without any overt toxicity. These results demonstrate that a unique formulation of a novel PI3-Kδ/HDAC6 dual inhibitor in combination with Navitoclax represents an approach for an efficient treatment option for ER breast cancer.
Journal • IO biomarker
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MYC (V-myc avian myelocytomatosis viral oncogene homolog) • BCL2 (B-cell CLL/lymphoma 2) • AKT1 (V-akt murine thymoma viral oncogene homolog 1)
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MYC overexpression • AKT1 overexpression
|
navitoclax (ABT 263)
over1year
DNASE1L3 inhibits hepatocellular carcinoma by delaying cell cycle progression through CDK2. (PubMed, Cell Oncol (Dordr))
Our study unveils DNASE1L3 as a novel HCC cell cycle regulator and tumor suppressor. DNASE1L3 impairs HCC tumorigenesis by delaying cell cycle progression possibly through disrupting the positive E2F1-CDK2 regulatory loop. DNASE1L3 may serve as a target for the development of novel therapeutic strategies against HCC.
Journal
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AKT1 (V-akt murine thymoma viral oncogene homolog 1) • CDK2 (Cyclin-dependent kinase 2) • E2F1 (E2F transcription factor 1)
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NRAS overexpression • AKT1 overexpression
over1year
miR-451a suppresses papillary thyroid cancer cell proliferation and invasion and facilitates apoptosis through targeting DCBLD2 and AKT1. (PubMed, Mol Cell Probes)
In addition, miR-451a reduced the growth of xenografted tumors in vivo. The data suggested that miR-451a attenuated the proliferation, invasion and promoted apoptosis in PTC cells via inhibiting DCBLD2 and AKT1.
Journal
|
MIR451A (MicroRNA 451a)
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AKT1 overexpression
over1year
Quatramer™ Mediated Codelivery of PI3-Kδ/HDAC6 Dual Inhibitor Augments the Anti-Cancer Efficacy of Epirubicin in Breast Cancer. (PubMed, Eur J Pharm Biopharm)
In comparison, the PI3-Kδ/HDAC6-NPs and Epi-NPs result in tumor growth inhibition of 15.86% and 81.59%, respectively. These studies predicted that clinical use of PI3-Kδ/HDAC6-Epi-NPs will be effective in breast cancer treatments.
Journal
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AKT1 (V-akt murine thymoma viral oncogene homolog 1)
|
AKT1 overexpression
almost2years
Anti‑oncogenic and pro‑myogenic action of the MKK6/p38/AKT axis induced by targeting MEK/ERK in embryonal rhabdomyosarcoma. (PubMed, Oncol Rep)
To the best of our knowledge, the present study demonstrates, for the first time, that the endogenous MKK6 pathway may be recovered by MEK/ERK inhibition (U0126 and trametinib) and that it concomitantly induces the reversal of the oncogenic pattern and the induction of the myogenic differentiation of ERMS cell lines. The effects of MEK/ERK inhibitors markedly increase the potential clinical applications in ERMS, particularly on account of the MEK inhibitor‑induced early MKK6/p38 axis activation and of their anti‑oncogenic effects. The findings presented herein lend further support to the antitumour effects of MKK6; MKK6 may thus represent a novel target for advanced personalised treatments against ERMS.
Journal
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MYC (V-myc avian myelocytomatosis viral oncogene homolog) • MAP2K3 (Mitogen-Activated Protein Kinase Kinase 3)
|
MYC expression • AKT1 overexpression
|
Mekinist (trametinib)
almost2years
Up-regulation of CPNE1 Appears to Enhance Cancer Progression in HER2-positive and Luminal A Breast Cancer Cells. (PubMed, Anticancer Res)
CPNE1 may play a key role in the pathophysiology of HER2-positive and luminal A subtypes of breast cancer.
Journal
|
HER-2 (Human epidermal growth factor receptor 2) • TYK2 (Tyrosine Kinase 2) • CPNE1 (Copine 1)
|
HER-2 positive • EGFR positive • AKT1 overexpression
almost2years
N(6)-methyladenosine-mediated miR-380-3p maturation and upregulation promotes cancer aggressiveness in pancreatic cancer. (PubMed, Bioengineered)
Moreover, the rescuing experiments validated that both PTEN overexpression and Akt pathway inhibitor LY294002 abrogated the promoting effects of miR-380-3p overexpression on cancer aggressiveness in PC cells. Collectively, this study firstly investigated the role of the m6A-associated miR-380-3p/PTEN/Akt pathway in regulating PC progression, which provided novel therapeutic and diagnostic biomarkers for this cancer.
Journal
|
METTL14 (Methyltransferase 14) • METTL3 (Methyltransferase Like 3)
|
AKT1 overexpression
|
LY294002
almost2years
METTL3 Promotes the Progression of Lung Cancer via Activating PI3K/AKT/mTOR Pathway. (PubMed, Clin Exp Pharmacol Physiol)
Elevated PI3K level then activates downstream AKT and mTOR signaling pathway and results in rapid cancer cell proliferation and metastasis. Taken together, our study reveals that METTL3-mediated m A methylation promotes lung cancer progression via activating PI3K/AKT/mTOR pathway.
Journal
|
METTL3 (Methyltransferase Like 3)
|
AKT1 overexpression
almost2years
DHW-221, a Dual PI3K/mTOR Inhibitor, Overcomes Multidrug Resistance by Targeting P-Glycoprotein (P-gp/ABCB1) and Akt-Mediated FOXO3a Nuclear Translocation in Non-small Cell Lung Cancer. (PubMed, Front Oncol)
Additionally, intragastrically administrated DHW-221 generated superior potency without obvious toxicity via FOXO3a nuclear translocation in an orthotopic A549/Taxol tumor mouse model. In conclusion, these results demonstrated that DHW-221, as a novel P-gp inhibitor, represents a prospective therapeutic candidate to overcome MDR in Taxol-resistant NSCLC treatment.
Journal
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AKT1 (V-akt murine thymoma viral oncogene homolog 1) • ABCB1 (ATP Binding Cassette Subfamily B Member 1) • FOXO3 (Forkhead box O3)
|
AKT1 overexpression
|
paclitaxel