ArticleCell death & disease2021
The role of E26 transformation-specific variant transcription factor 5 in colorectal cancer cell proliferation and cell cycle progression.
Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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16 citing papers in PubMed, 18 citations in OpenAlex.
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- Global DNA methylation signatures associated with chemoresistance and poor prognosis of high grade serous ovarian cancer.Scientific reports · 2025Article
- The role of the transcription factor PATZ1 in tumorigenesis and metabolic regulation.Journal of cancer research and clinical oncology · 2025Review
- Liraglutide inhibits the development of colorectal cancer by regulating TGF-β/Smad3 signaling pathway and affecting epithelial-mesenchymal transition.Discover oncology · 2025Article
- Transcriptional regulation of ETV5 by mitogen-activated protein kinase via ETS-1 in human pancreatic cancer cells.Scientific reports · 2025Article
- Identification of ETV5 as a prognostic marker related to epigenetic modification in pan-cancer and facilitates tumor progression in hepatocellular carcinoma.Scientific reports · 2024Article
- Innovative prognostic modeling in ESCC: leveraging scRNA-seq and bulk-RNA for dendritic cell heterogeneity analysis.Frontiers in immunology · 2024Article
- ETV5 regulates proliferation and cell cycle genes in the INS-1 (832/13) cell line independently of the concentration of secreted insulin.FEBS open bio · 2023Article
- Lappaol F regulates the cell cycle by activating CDKN1C/p57 in human colorectal cancer cells.Pharmaceutical biology · 2023Article
- A novel nomogram based on cell cycle-related genes for predicting overall survival in early-onset colorectal cancer.BMC cancer · 2023Article
- The Functional Role and Regulatory Mechanism of FTO mInternational journal of molecular sciences · 2023Article
- E26 transformation-specific transcription variant 5 in development and cancer: modification, regulation and function.Journal of biomedical science · 2023Review
- Article
- ETV5 overexpression promotes progression of esophageal squamous cell carcinoma by upregulating SKA1 and TRPV2.International journal of medical sciences · 2022Article
- Effects of GLP-1 Receptor Agonists on Biological Behavior of Colorectal Cancer Cells by Regulating PI3K/AKT/mTOR Signaling Pathway.Frontiers in pharmacology · 2022Article
- ETV1 Positively Correlated With Immune Infiltration and Poor Clinical Prognosis in Colorectal Cancer.Frontiers in immunology · 2022Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
E26 transformation-specific variant transcription factor 5 (ETV5) contributes to tumor growth and progression and promotes colorectal cancer (CRC) angiogenesis. Previous studies indicate that ETV5 may regulate the cell cycle, but its detailed mechanism remain unclear. Gene Ontology (GO) analysis of RNA-seq data revealed that ETV5 possibly regulates the cell cycle in CRC. Here, in vitro and in vivo experiments were performed to verify that ETV5 promoted tumor progression and influenced cell cycle G1/S transition. Cell cycle PCR array and co-immunoprecipitation (Co-IP) helped identify the p21-CDKs pathway. Chromatin immunoprecipitation (ChIP) and luciferase reporter assays were performed to determine whether ETV5 binds to the p21 promoter. ETV5 and p21 were detected by immunohistochemistry, and the effects of their expression on CRC patients were evaluated. ETV5 upregulation enhanced tumor proliferative capacity and promoted G1 phase transfer to the S phase. ETV5 knockdown slowed the growth of CRC cells and repressed the G1/S transition. We also found p21 as a downstream target of ETV5. p21 knockdown resulted in faster CRC cell growth and in more cells being driven from the G0/1 phase into the S phase. Co-IP experiments showed that p21 banding to CDK2, CDK4, and CDK6 inhibited p130 phosphorylation. Using the ChIP and luciferase reporter assay, we confirmed that ETV5 bound to the p21 promoter and repressed p21 expression. CRC patients with high ETV5 expression and low p21 expression showed the worst prognosis. Finally, by targeting p21 to regulate CDK function, ETV5 also changed drug-sensitivity to palbociclib and dinaciclib. In conclusion, ETV5 promoted cell cycle G1/S transition through transcriptional inhibition of p21, thereby accelerating tumor growth. Moreover, ETV5 changed drug-sensitivity to palbociclib and dinaciclib. Therefore, therapeutic regimens targeting ETV5 may be promising in improving the efficacy of target-CDK treatment in CRC.
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