ArticleMolecular and cellular biology2005
BAF57 governs androgen receptor action and androgen-dependent proliferation through SWI/SNF.
Article in Molecular and cellular biology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.
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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.
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Who cites it
62 citing papers in PubMed, 127 citations in OpenAlex.
- The TRIP12 E3 ligase induces SWI/SNF component BRG1-β-catenin interaction to promote Wnt signaling.Nature communications · 2025Article
- Targeting SWI/SNF Complexes in Cancer: Pharmacological Approaches and Implications.Epigenomes · 2024Review
- SWI/SNF chromatin remodelers in prostate cancer progression.Frontiers in epigenetics and epigenomics · 2023Review
- Epigenetic Coregulation of Androgen Receptor Signaling.Advances in experimental medicine and biology · 2022Article
- To bind or not to bind: Cistromic reprogramming in prostate cancer.Frontiers in oncology · 2022Review
- Role of Peroxisome Proliferator-Activated Receptors (PPARs) in Energy Homeostasis of Dairy Animals: Exploiting Their Modulation through Nutrigenomic Interventions.International journal of molecular sciences · 2021Review
- Chromatin and Epigenetic Dysregulation of Prostate Cancer Development, Progression, and Therapeutic Response.Cancers · 2021Review
- Article
- Loss of SWI/SNF Chromatin Remodeling Alters NRF2 Signaling in Non-Small Cell Lung Carcinoma.Molecular cancer research : MCR · 2020Article
- BRM: the core ATPase subunit of SWI/SNF chromatin-remodelling complex-a tumour suppressor or tumour-promoting factor?Epigenetics & chromatin · 2019Review
- Unwinding chromatin at the right places: how BAF is targeted to specific genomic locations during development.Development (Cambridge, England) · 2019Review
- smarce1 mutants have a defective endocardium and an increased expression of cardiac transcription factors in zebrafish.Scientific reports · 2018Article
- Rationale for the development of alternative forms of androgen deprivation therapy.Endocrine-related cancer · 2017Review
- SMARCE1 is required for the invasive progression of in situ cancers.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Review
- Progesterone receptor blockade in human breast cancer cells decreases cell cycle progression through G2/M by repressing G2/M genes.BMC cancer · 2016Article
- The BAF chromatin remodelling complex is an epigenetic regulator of lineage specification in the early mouse embryo.Development (Cambridge, England) · 2016Article
- Glucocorticoid Receptor Transcriptional Activation via the BRG1-Dependent Recruitment of TOP2β and Ku70/86.Molecular and cellular biology · 2015Article
- Expression of BAF57 in ovarian cancer cells and drug sensitivity.Cancer science · 2015Article
- HMGB1 in health and disease.Molecular aspects of medicine · 2014Review
2 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Androgen receptor (AR) activity is required for prostate cancer development and progression. Thus, there is a major impetus to understand the regulation of AR action. We and others have previously shown that AR transactivation potential is dependent on the presence of an active SWI/SNF chromatin remodeling complex. However, the mechanisms underlying SWI/SNF regulation of the AR remained unsolved. We show here that the BAF57 subunit, an accessory component of the remodeling complex, is a critical regulator of AR function. We show that BAF57 is expressed in the luminal epithelia of the prostate and is required for AR-dependent transactivation in prostatic adenocarcinoma cells. Our data reveal that BAF57 can directly bind to the AR and is recruited to endogenous AR targets upon ligand activation. Loss of BAF57 or inhibition of BAF57 function severely compromised AR activity, as observed with both exogenous and endogenous AR targets. Rescue of BAF57 function restored AR activity, thus demonstrating a specific requirement of BAF57 for AR activity. This action of BAF57 proved to be dependent on SWI/SNF ATPase function. BAF57 has previously been implicated in nuclear receptor coactivator function, and we show that, although BAF57 facilitated coactivator activity, only a selected subset required BAF57 for coactivator function. Lastly, we demonstrate that both BAF57 and BRM are required for the proliferation of AR-dependent prostatic adenocarcinoma cells. In summary, these findings identify BAF57 as a critical modulator of the AR that is capable of altering AR activity, coactivator function, and AR-dependent proliferation.
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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.