ArticleCarcinogenesis2008
Prohibitin and the SWI/SNF ATPase subunit BRG1 are required for effective androgen antagonist-mediated transcriptional repression of androgen receptor-regulated genes.
Article in Carcinogenesis, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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
42 citing papers in PubMed, 67 citations in OpenAlex.
- Profiling HIV1-host protein-protein interaction networks in patient-derived exosome proteins: impact on pathophysiology and innate immune pathways.Virology journal · 2025Article
- Prostate cancer exploits BRD9-driven metabolic reprogramming to shape the aggressive phenotype.Cell death & disease · 2025Article
- Emerging roles of prohibitins in cancer: an update.Cancer gene therapy · 2025Review
- SWI/SNF-type complexes-transcription factor interplay: a key regulatory interaction.Cellular & molecular biology letters · 2025Review
- Low SMARCD3 expression is associated with poor prognosis in patients with prostate cancer.The Prostate · 2025Article
- SWI/SNF Complex Connects Signaling and Epigenetic State in Cells of Nervous System.Molecular neurobiology · 2025Review
- Rational Design and Development of Selective BRD7 Bromodomain Inhibitors and Their Activity in Prostate Cancer.Journal of medicinal chemistry · 2023Article
- Targeting PHB1 to inhibit castration-resistant prostate cancer progression in vitro and in vivo.Journal of experimental & clinical cancer research : CR · 2023Article
- SWI/SNF chromatin remodelers in prostate cancer progression.Frontiers in epigenetics and epigenomics · 2023Review
- Article
- OTUD6A promotes prostate tumorigenesis via deubiquitinating Brg1 and AR.Communications biology · 2022Article
- BRG1 knockdown inhibits proliferation through multiple cellular pathways in prostate cancer.Clinical epigenetics · 2021Article
- BRG1 Activates Proliferation and Transcription of Cell Cycle-Dependent Genes in Breast Cancer Cells.Cancers · 2020Article
- BRM: the core ATPase subunit of SWI/SNF chromatin-remodelling complex-a tumour suppressor or tumour-promoting factor?Epigenetics & chromatin · 2019Review
- Prohibitin: a prime candidate for a pleiotropic effector that mediates sex differences in obesity, insulin resistance, and metabolic dysregulation.Biology of sex differences · 2019Review
- The prohibitin-repressive interaction with E2F1 is rapidly inhibited by androgen signalling in prostate cancer cells.Oncogenesis · 2017Article
- Prohibitin promotes androgen receptor activation in ER-positive breast cancer.Cell cycle (Georgetown, Tex.) · 2017Article
- Extensive cargo identification reveals distinct biological roles of the 12 importin pathways.eLife · 2017Article
- Evaluation of the role of downregulation of SNF5/INI1 core subunit of SWI/SNF complex in clear cell renal cell carcinoma development.American journal of cancer research · 2017Article
- Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Androgen antagonists or androgen deprivation are the primary therapeutic modalities for the treatment of prostate cancer. Invariably, however, the disease becomes progressive and unresponsive to androgen ablation therapy (hormone refractory). The molecular mechanisms by which androgen antagonists inhibit prostate cancer proliferation are not fully defined. In this study, we identify two molecules which are required for effective prostate cancer cell responsiveness to androgen antagonists. We establish that androgen receptor (AR)-dependent transcriptional suppression by androgen antagonists requires the tumor suppressor prohibitin. This requirement for prohibitin was demonstrated using structurally-distinct androgen antagonists, stable and transient knockdown of prohibitin and transfected and endogenous AR-responsive genes. The SWI-SNF complex core ATPase BRG1, but not its closely-related counterpart ATPase BRM, is required for this repressive action of prohibitin on AR-responsive promoters. Androgen antagonists induce recruitment of prohibitin and BRG1 to endogenous AR-responsive promoters and induce a physical association between AR and prohibitin and BRG1. The recruitment of prohibitin to endogenous AR-responsive promoters is dependent upon antagonist-bound AR. Prohibitin binding in the prostate-specific antigen (PSA) promoter results in the recruitment of BRG1 and the dissociation of p300 from the PSA promoter. These findings suggest that prohibitin may function through BRG1-mediated local chromatin remodeling activity and the removal of p300-mediated acetylation to produce androgen antagonist-mediated transcriptional repression. Furthermore, in addition to its necessary role in AR-mediated transcriptional repression, we demonstrate that prohibitin is required for full and efficient androgen antagonist-mediated growth suppression of prostate cancer cells.
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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.