ArticleThe Prostate2015
Androgen receptor splice variants contribute to prostate cancer aggressiveness through induction of EMT and expression of stem cell marker genes.
Article in The Prostate, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.
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Who cites it
65 citing papers in PubMed, 111 citations in OpenAlex.
- Lathyrol affects the expression of AR and PSA and inhibits the malignant behavior of RCC cells.Open medicine (Warsaw, Poland) · 2025Article
- Caffeic acid phenethyl ester suppresses the expression of androgen receptor variant 7 via inhibition of CDK1 and AKT.Cancer gene therapy · 2024Article
- Review
- Prostate Cancer Stem Cells: Biology and Treatment Implications.International journal of molecular sciences · 2023Review
- A role for androgen receptor variant 7 in sensitivity to therapy: Involvement of IGFBP-2 and FOXA1.Translational oncology · 2023Article
- Therapeutic implications of cancer stem cells in prostate cancer.Cancer biology & medicine · 2023Review
- Murine toxicology and pharmacokinetics of lead next generation galeterone analog, VNPP433-3β.Steroids · 2023Article
- Zinc finger protein‑like 1 is a novel neuroendocrine biomarker for prostate cancer.International journal of oncology · 2023Article
- Racial Differences in Androgen Receptor (AR) and AR Splice Variants (AR-SVs) Expression in Treatment-Naïve Androgen-Dependent Prostate Cancer.Biomedicines · 2023Article
- Therapeutic targeting of histone lysine demethylase KDM4B blocks the growth of castration-resistant prostate cancer.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2023Article
- Emergent dynamics of underlying regulatory network links EMT and androgen receptor-dependent resistance in prostate cancer.Computational and structural biotechnology journal · 2023Article
- Stem Cells as Target for Prostate cancer Therapy: Opportunities and Challenges.Stem cell reviews and reports · 2022Review
- Constitutively Active Androgen Receptor in Hepatocellular Carcinoma.International journal of molecular sciences · 2022Review
- Liquid biopsy-based targeted gene screening highlights tumor cell subtypes in patients with advanced prostate cancer.Clinical and translational science · 2022Article
- Phloretin in Benign Prostate Hyperplasia and Prostate Cancer: A Contemporary Systematic Review.Life (Basel, Switzerland) · 2022Review
- Androgen receptor-mediated transcriptional repression targets cell plasticity in prostate cancer.Molecular oncology · 2022Article
- Unexplored Functions of Sex Hormones in Glioblastoma Cancer Stem Cells.Endocrinology · 2022Review
- Prostate Cancer Stem Cells: Clinical Aspects and Targeted Therapies.Frontiers in oncology · 2022Review
- Non-Coding RNAs Set a New Phenotypic Frontier in Prostate Cancer Metastasis and Resistance.International journal of molecular sciences · 2021Review
- Regulation of carcinogenesis and mediation through Wnt/β-catenin signaling by 3,3'-diindolylmethane in an enzalutamide-resistant prostate cancer cell line.Scientific reports · 2021Article
5 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundThe mechanism(s) by which androgen receptor (AR) splice variants contribute to castration-resistant prostate cancer (CRPC) is still lacking.
methodsExpressions of epithelial-to-mesenchymal transition (EMT) and stem cell markers were molecularly tested using prostate cancer (PCa) cells transfected with AR and AR3 (also known as AR-V7) plasmids or siRNA, and also cultured cells under androgen deprivation therapy (ADT) condition. Cell migration, clonogenicity, sphere-forming capacity was assessed using PCa cells under all experimental conditions and 3,3'-diindolylmethane (DIM; BR-DIM) treatment. Human PCa samples from BR-DIM untreated or treated patients were also used for assessing the expression of AR3 and stem cell markers.
resultsOverexpression of AR led to the induction of EMT phenotype, while overexpression of AR3 not only induced EMT but also led to the expression of stem cell signature genes. More importantly, ADT enhanced the expression of AR and AR3 concomitant with up-regulated expression of EMT and stem cell marker genes. Dihydrotestosterone (DHT) treatment decreased the expression of AR and AR3, and reversed the expression of these EMT and stem cell marker genes. BR-DIM administered to PCa patients prior to radical prostatectomy inhibited the expression of cancer stem cell markers consistent with inhibition of self-renewal of PCa cells after BR-DIM treatment.
conclusionAR variants could contribute to PCa progression through induction of EMT and acquisition of stem cell characteristics, which could be attenuated by BR-DIM, suggesting that BR-DIM could become a promising agent for the prevention of CRPC and/or for the treatment of PCa.
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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.