ArticleOncogene2004
Androgens repress Bcl-2 expression via activation of the retinoblastoma (RB) protein in prostate cancer cells.
Article in Oncogene, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 56 citations in OpenAlex.
- Single-cell imaging analysis, therapeutic modeling and a Phase Ib trial validate BCL-2 as a target across heterogeneous castration-resistant prostate cancer.Signal transduction and targeted therapy · 2026Trial
- Breaking the bonds: targeting protein dimerization for prostate cancer therapy.Endocrinology · 2026Review
- Phase Ib study of enzalutamide with venetoclax in patients with metastatic castration-resistant prostate cancer.Cancer chemotherapy and pharmacology · 2025Article
- Evodiamine induces ferroptosis in prostate cancer cells by inhibiting TRIM26-mediated stabilization of GPX4.Chinese medicine · 2025Article
- Heterogeneous Responses to High-Dose Testosterone in Castration-Resistant Prostate Cancer Tumors with Mixed Rb-Proficient and Rb-Deficient Cells.Molecular cancer therapeutics · 2025Article
- BCL2 expression is enriched in advanced prostate cancer with features of lineage plasticity.The Journal of clinical investigation · 2024Article
- Current use of androgens in bone marrow failure disorders: a report from the Severe Aplastic Anemia Working Party of the European Society for Blood and Marrow Transplantation.Haematologica · 2024Article
- Sanguinarine chloride induces ferroptosis by regulating ROS/BACH1/HMOX1 signaling pathway in prostate cancer.Chinese medicine · 2024Article
- Exploiting the tumor-suppressive activity of the androgen receptor by CDK4/6 inhibition in castration-resistant prostate cancer.Molecular therapy : the journal of the American Society of Gene Therapy · 2022Article
- High-dose-androgen-induced autophagic cell death to suppress the Enzalutamide-resistant prostate cancer growth via altering the circRNA-BCL2/miRNA-198/AMBRA1 signaling.Cell death discovery · 2022Article
- Targeting the Intrinsic Apoptosis Pathway: A Window of Opportunity for Prostate Cancer.Cancers · 2021Review
- Suppressing BCL-XL increased the high dose androgens therapeutic effect to better induce the Enzalutamide-resistant prostate cancer autophagic cell death.Cell death & disease · 2021Article
- Linking prostate cancer cell AR heterogeneity to distinct castration and enzalutamide responses.Nature communications · 2018Article
- Sensitisation to mitoxantrone-induced apoptosis by the oncolytic adenovirus Ad∆∆ through Bcl-2-dependent attenuation of autophagy.Oncogenesis · 2018Article
- Bcl-2 expression is a poor predictor for hepatocellular carcinoma prognosis of andropause-age patients.Cancer biology & medicine · 2016Article
- P300 acetyltransferase regulates fatty acid synthase expression, lipid metabolism and prostate cancer growth.Oncotarget · 2016Article
- Disruptive environmental chemicals and cellular mechanisms that confer resistance to cell death.Carcinogenesis · 2015Review
- Oxymatrine downregulates HPV16E7 expression and inhibits cell proliferation in laryngeal squamous cell carcinoma Hep-2 cells in vitro.BioMed research international · 2015Article
- DNA damage-binding complex recruits HDAC1 to repress Bcl-2 transcription in human ovarian cancer cells.Molecular cancer research : MCR · 2014Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The oncogene Bcl-2 is upregulated frequently in prostate tumors following androgen ablation therapy, and Bcl-2 overexpression may contribute to the androgen-refractory relapse of the disease. However, the molecular mechanism underlying androgenic regulation of Bcl-2 in prostate cancer cells is understood poorly. In this study, we demonstrated that no androgen response element (ARE) was identified in the androgen-regulated region of the P1 promoter of Bcl-2 gene, whereas, we provided evidence that the androgenic effect is mediated by E2F1 protein through a putative E2F-binding site in the promoter. We further demonstrated that retinoblastoma (RB) protein plays a critical role in androgen regulation of Bcl-2. The phosphorylation levels of RB at serine residues 780 and 795 were decreased in LNCaP cells treated with androgens. Ectopic expression of a constitutively active form of RB inhibited expression of Bcl-2. Knockdown of endogenous RB protein by an Rb small inference RNA (siRNA) induced an increase in Bcl-2 levels. Most importantly, the effect of androgens on Bcl-2 was abolished completely by specific inhibition of RB function with a mutated E1A. Finally, androgen treatment of LNCaP cells upregulated specifically levels of the cyclin-dependent kinase inhibitors (CDKIs) p15INK4B and p27KIP1. Ectopic expression of p15INK4B and/or p27KIP1 inhibited Bcl-2 expression. Knockdown of endogenous p15INK4B or p27KIP1 protein with a pool of siRNAs diminished androgen-induced downregulation of Bcl-2 expression. Therefore, our data indicate that androgens suppress Bcl-2 expression through negatively modulating activities of the E2F site in the Bcl-2 promoter by activating the CDKI-RB axis.
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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.