ArticleThe Journal of biological chemistry2014
Androgen receptor splice variant AR3 promotes prostate cancer via modulating expression of autocrine/paracrine factors.
Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
What it found
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
56 citing papers in PubMed, 91 citations in OpenAlex.
- Alterations in AR-FOXA1 signaling in prostate cancer progression and therapeutic resistance.Journal of the National Cancer Center · 2026Review
- Interactions between androgen and IGF1 axes in prostate tumorigenesis.Nature reviews. Urology · 2025Review
- Case report and literature review of rezvilutamide in the treatment of hormone-sensitive prostate cancer.Frontiers in oncology · 2024Article
- Review
- Beyond Prostate Cancer: An Androgen Receptor Splice Variant Expression in Multiple Malignancies, Non-Cancer Pathologies, and Development.Biomedicines · 2023Review
- A role for androgen receptor variant 7 in sensitivity to therapy: Involvement of IGFBP-2 and FOXA1.Translational oncology · 2023Article
- Androgen receptor variant 7 exacerbates hepatocarcinogenesis in a c-MYC-driven mouse HCC model.Oncogenesis · 2023Article
- Aberrant androgen action in prostatic progenitor cells induces oncogenesis and tumor development through IGF1 and Wnt axes.Nature communications · 2022Article
- Anti-Androgen Receptor Therapies in Prostate Cancer: A Brief Update and Perspective.Frontiers in oncology · 2022Review
- Alternative RNA splicing in tumour heterogeneity, plasticity and therapy.Disease models & mechanisms · 2022Review
- Suspension state regulates epithelial-to-mesenchymal transition and stemness of breast tumor cells.Biotechnology letters · 2021Article
- Noncoding RNAs regulate alternative splicing in Cancer.Journal of experimental & clinical cancer research : CR · 2021Review
- Protein Expression Analysis of an In Vitro Murine Model of Prostate Cancer Progression: Towards Identification of High-Potential Therapeutic Targets.Journal of personalized medicine · 2020Article
- Cellular rewiring in lethal prostate cancer: the architect of drug resistance.Nature reviews. Urology · 2020Review
- Article
- Ambra1 induces autophagy and desensitizes human prostate cancer cells to cisplatin.Bioscience reports · 2019Article
- Genetically Engineered Mouse Models of Prostate Cancer in the Postgenomic Era.Cold Spring Harbor perspectives in medicine · 2019Review
- Androgen receptor splice variant-7 expression emerges with castration resistance in prostate cancer.The Journal of clinical investigation · 2019Article
- EMT Markers in Locally-Advanced Prostate Cancer: Predicting Recurrence?Frontiers in oncology · 2019Article
- RNA Splicing and Disease: Animal Models to Therapies.Trends in genetics : TIG · 2019Review
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 1 country.
Funding
Abstract
Deregulation of androgen receptor (AR) splice variants has been implicated to play a role in prostate cancer development and progression. To understand their functions in prostate, we established a transgenic mouse model (AR3Tg) with targeted expression of the constitutively active and androgen-independent AR splice variant AR3 (a.k.a. AR-V7) in prostate epithelium. We found that overexpression of AR3 modulates expression of a number of tumor-promoting autocrine/paracrine growth factors (including Tgfβ2 and Igf1) and expands prostatic progenitor cell population, leading to development of prostatic intraepithelial neoplasia. In addition, we showed that some epithelial-mesenchymal transition-associated genes are up-regulated in AR3Tg prostates, suggesting that AR3 may antagonize AR activity and halt the differentiation process driven by AR and androgen. This notion is supported by our observations that the number of Ck5(+)/Ck8(+) intermediate cells is increased in AR3Tg prostates after castration, and expression of AR3 transgene in these intermediate cells compromises prostate epithelium regeneration upon androgen replacement. Our results demonstrate that AR3 is a driver of prostate cancer, at least in part, through modulating multiple tumor-promoting autocrine/paracrine factors.
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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.