{
  "id": 15540833,
  "title": "cBAF drives AR-V7 expression through regulation of transcriptional termination in castration-resistant prostate cancer",
  "url": "https://urgent.news/2026/10/18/cbaf-drives-ar-v7-expression-through-regulation-of-transcriptional",
  "topic": "health",
  "section": "Health & Medicine",
  "published": "2026-10-18T00:00:00.000Z",
  "source": {
    "name": "bioRxiv",
    "slug": "biorxiv",
    "url": "https://www.biorxiv.org/content/10.64898/2026.10.13.758074v1?rss=1"
  },
  "original_language": "en",
  "account": "Androgen receptor splice variant AR-V7 fuels resistance to targeted therapies in advanced prostate cancer, yet the forces controlling its production remain elusive. Researchers have now pinpointed the cBAF chromatin remodeling complex as a key player in governing AR-V7 expression. By disabling cBAF through pharmacological or genetic means, they observed a drop in AR-V7 levels, a halt in AR-V7-driven transcriptional activity, and a decline in prostate cancer cell growth.\n\nAt the molecular level, cBAF latches onto an intronic regulatory region nestled downstream of AR cryptic exon 3. Here, it keeps the chromatin open, boosts enhancer activity, and links the promoter to an enhancer. Without cBAF, the transcription termination machinery is less likely to show up, RNA polymerase II Thr4 phosphorylation is reduced, and transcription extends past the AR-V7 polyadenylation site. By tracking RNA transcripts, the team discovered that cBAF-driven termination is essential for AR-V7 production and fine-tunes termination at select genes across the genome.\n\nThese results shed light on how cBAF orchestrates chromatin-level control of transcriptional termination, establishing it as a pivotal factor in dictating AR-V7 levels in castration-resistant prostate cancer.",
  "summary": "The androgen receptor splice variant AR-V7 drives resistance to androgen receptor-targeted therapies in castration-resistant prostate cancer (CRPC), but the mechanisms governing its expression remain incompletely understood. Here, we identify the canonical BAF (cBAF) chromatin remodeling complex as a selective regulator of AR-V7 expression. Pharmacologic and genetic disruption of cBAF reduced…",
  "key_points": [],
  "editors_take": null,
  "illustration": null,
  "coverage": {
    "outlets": 1,
    "also_reported_by": []
  },
  "ai_generated": true,
  "disclaimer": "Summaries, key points and the editor’s take are written by software from other outlets’ reporting and may contain errors — always check the linked original."
}