ArticleOncogenesis2012
Overexpression of ETV4 is oncogenic in prostate cells through promotion of both cell proliferation and epithelial to mesenchymal transition.
Article in Oncogenesis, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed, 73 citations in OpenAlex.
- TMPRSS2-ERG confers resistance of prostate cancer to antiandrogens.EMBO molecular medicine · 2026Article
- Emerging role of ETV4 in colorectal cancer: from molecular mechanisms to clinical implications.Frontiers in oncology · 2026Review
- Oncogenic Fusions HarboringCancers · 2025Review
- A novel deep learning framework with dynamic tokenization for identifying chromatin interactions along with motif importance investigation.Briefings in bioinformatics · 2025Article
- PEA3 Transcription Factors, Role in Invasion, Proliferation and Radioresistance of Glioblastoma Stem Cells.Journal of cellular and molecular medicine · 2025Article
- Impairment of DET1 causes neurological defects and lethality in mice and humans.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Comprehensive analysis of the functional and immunological significance of ETV4 in pan-cancer and its validation in digestive tumors.Frontiers in immunology · 2025Article
- Interactions of Polychlorinated Biphenyls and Their Metabolites with the Brain and Liver Transcriptome of Female Mice.ACS chemical neuroscience · 2024Article
- A Lipopeptidomimetic of Transcriptional Activation Domains Selectively Disrupts the Coactivator Med25 Protein-Protein Interactions.Angewandte Chemie (International ed. in English) · 2024Article
- Article
- Identification and characterization of novel ETV4 splice variants in prostate cancer.Scientific reports · 2023Article
- Down-regulated MiRNA 29-b as a diagnostic marker in colorectal cancer and its correlation with ETV4 and Cyclin D1 immunohistochemical expression.Cancer biomarkers : section A of Disease markers · 2023Article
- Portrait of Molecular Signaling and Putative Therapeutic Targets in Prostate Cancer withBiomedicines · 2022Article
- Reliable epithelial-mesenchymal transition biomarkers for colorectal cancer detection.Biomarkers in medicine · 2022Article
- Allelic imbalance of chromatin accessibility in cancer identifies candidate causal risk variants and their mechanisms.Nature genetics · 2022Article
- Computing microRNA-gene interaction networks in pan-cancer using miRDriver.Scientific reports · 2022Article
- E26 transformation-specific variant 4 as a tumor promotor in human cancers through specific molecular mechanisms.Molecular therapy oncolytics · 2021Review
- Norstictic Acid Is a Selective Allosteric Transcriptional Regulator.Journal of the American Chemical Society · 2021Article
- ETV4 promotes breast cancer cell stemness by activating glycolysis and CXCR4-mediated sonic Hedgehog signaling.Cell death discovery · 2021Article
- ETV4 plays a role on the primary events during the adenoma-adenocarcinoma progression in colorectal cancer.BMC cancer · 2021Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The discovery of translocations that involve one of the genes of the ETS family (ERG, ETV1, ETV4 and ETV5) has been a major advance in understanding the molecular basis of prostate cancer (PC). Each one of these translocations results in deregulated expression of one of the ETS proteins. Here, we focus on the mechanism whereby overexpression of the ETV4 gene mediates oncogenesis in the prostate. By siRNA technology, we show that ETV4 inhibition in the PC3 cancer cell line reduces not only cell mobility and anchorage-independent growth, but also cell proliferation, cell cycle progression and tumor growth in a xenograft model. Conversely, ETV4 overexpression in the nonmalignant human prostate cell line (RWPE) increases anchorage-independent growth, cell mobility and cell proliferation, which is probably mediated by downregulation of p21, producing accelerated progression through the cell cycle. ETV4 overexpression is associated with changes in the pattern of E-cadherin and N-cadherin expression; the cells also become spindle-shaped, and these changes are characteristic of the so-called epithelial to mesenchymal transition (EMT). In RWPE cells overexpressing ETV4 EMT results from a marked increase in EMT-specific transcription factors such as TWIST1, SLUG1, ZEB1 and ZEB2. Thus, whereas ETV4 shares with the other ETS proteins (ERG, ETV5 and ETV1) a major role in invasiveness and cell migration, it emerges as unique in that it increases at the same time also the rate of proliferation of PC cells. Considering the wide spectrum in the clinical course of patients with PC, it may be highly relevant that ETV4 is capable of inducing most and perhaps all of the features that make a tumor aggressive.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.