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Constitutively active AR splice variants (AR-Vs), such as AR-V7, play a key role in driving treatment resistance and disease progression. Importantly, the failure to attenuate AR-V function represents a major unmet clinical need, and as such, defining how AR-Vs are generated is likely to yield new therapeutic targets. Our knowledge of factors that mediate splicing of AR-V\u2013encoding mRNAs remains limited. Here, we have employed an RNA-targeting CasRx approach to identify selective protein interactors of\n                    <jats:italic>AR-V7<\/jats:italic>\n                    mRNA in PC. TRA2B and its ortholog, TRA2A, were identified as splicing regulators of\n                    <jats:italic>AR<\/jats:italic>\n                    transcripts that facilitate AR-V synthesis at the expense of full-length AR isoforms. TRA2B expression correlated with\n                    <jats:italic>AR-V7<\/jats:italic>\n                    transcript in CRPC and attenuation of TRA2-mediated splicing diminished PC cell growth. Exploiting TRA2B function may therefore provide new therapeutic opportunities in advanced disease.\n                  <\/jats:p>","DOI":"10.1172\/jci198264","type":"journal-article","created":{"date-parts":[[2026,3,31]],"date-time":"2026-03-31T18:00:57Z","timestamp":1774980057000},"source":"Crossref","is-referenced-by-count":2,"title":["Splicing factor TRA2B enhances synthesis of androgen receptor variant AR-V7 in prostate cancer cells"],"prefix":"10.1172","volume":"136","author":[{"given":"Nicholas","family":"Brittain","sequence":"first","affiliation":[{"name":"Newcastle University Centre for Cancer, Paul O\u2019Gorman Building, Framlington Place, Newcastle upon Tyne, United Kingdom."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9566-5096","authenticated-orcid":true,"given":"Alec","family":"Paschalis","sequence":"additional","affiliation":[{"name":"The Institute for Cancer Research, London, United Kingdom."},{"name":"The Royal Marsden 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