ArticleProceedings of the National Academy of Sciences of the United States of America2009
ETS family transcription factors collaborate with alternative signaling pathways to induce carcinoma from adult murine prostate cells.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 127 papers, 2 of them syntheses that pooled it.
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Who cites it
127 citing papers in PubMed, 2 syntheses or guidelines pooled it, 200 citations in OpenAlex.
- Loss of the NKX3.1 tumorsuppressor promotes the TMPRSS2-ERG fusion gene expression in prostate cancer.BMC cancer · 2014Pooled it
- Prevalence and clinical application ofAsian journal of andrologyPooled it
- The prognostic significance of combined ERG and androgen receptor expression in patients with prostate cancer managed by androgen deprivation therapy.Cancer biology & therapy · 2014Trial
- ERG function in prostate cells is regulated by distinct positive feedback loops depending on AKT signaling status.Research square · 2026Article
- Androgen deprivation-mediated activation of AKT is enhanced in prostate cancer with TMPRSS2:ERG fusion.The Journal of clinical investigation · 2025Article
- Deciphering the Transcription Factor Landscape in Prostate Cancer Progression: A Novel Approach to Understand NE Transdifferentiation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- The Role of Induced Pluripotent Stem Cells in the Treatment of Stroke.Current neuropharmacology · 2024Review
- Article
- ETV4 mediates dosage-dependent prostate tumor initiation and cooperates with p53 loss to generate prostate cancer.Science advances · 2023Article
- ETS factors in prostate cancer.Cancer letters · 2022Review
- Review
- Discovery proteomics defines androgen-regulated glycoprotein networks in prostate cancer cells, as well as putative biomarkers of prostatic diseases.Scientific reports · 2021Article
- Oncogenic gene fusions in nonneoplastic precursors as evidence that bacterial infection can initiate prostate cancer.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Ras/ERK and PI3K/AKT signaling differentially regulate oncogenic ERG mediated transcription in prostate cells.PLoS genetics · 2021Article
- Cooperation between ETS transcription factor ETV1 and histone demethylase JMJD1A in colorectal cancer.International journal of oncology · 2020Article
- Targetable gene fusions and aberrations in genitourinary oncology.Nature reviews. Urology · 2020Review
- ETV4 promotes late development of prostatic intraepithelial neoplasia and cell proliferation through direct and p53-mediated downregulation of p21.Journal of hematology & oncology · 2020Article
- Therapies Targeted to Androgen Receptor Signaling Axis in Prostate Cancer: Progress, Challenges, and Hope.Cancers · 2019Review
- TMPRSS2-ERG fusions confer efficacy of enzalutamide in an in vivo bone tumor growth model.BMC cancer · 2019Article
- Strong cytoplasmic ETV1 expression has a negative impact on prostate cancer outcome.Virchows Archiv : an international journal of pathology · 2019Article
67 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
Chromosomal rearrangements involving erythroblast transformation specific (ETS) family transcription factors were recently defined as the most common genetic alterations in human prostate cancer. Despite their prevalence, it is unclear what quantitative role they play in either initiation or progression of the disease. Using a lentiviral transduction and dissociated cell prostate regeneration approach, we find that acutely increased expression of ETS proteins in adult murine prostate epithelial cells is sufficient to induce the formation of epithelial hyperplasia and focal prostatic intraepithelial neoplasia (PIN) lesions, but not progression to carcinoma. However, combined expression of ERG with additional genetic alternations associated with human prostate cancer can lead to aggressive disease. Although ERG overexpression does not cooperate with loss of the tumor suppressor p53, it does collaborate with alterations in PI3K signaling, such as Pten knockdown or AKT up-regulation, to produce a well-differentiated adenocarcinoma. Most striking is our finding that overexpression of androgen receptor (AR) does not give rise to any hyperplastic lesions, but when combined with high levels of ERG, it promotes the development of a more poorly differentiated, invasive adenocarcinoma. These findings suggest that in human prostate cancer, the most potent function of ETS gene fusions may be to synergize with alternative genetic events and provide different pathways for carcinoma production and invasive behavior. Our results provide direct evidence for selective cooperating events in ERG-induced prostate tumorigenesis and offer a rational basis for combined therapeutic interventions against multiple oncogenic pathways in prostate cancer.
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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.