ArticleInternational journal of general medicine2026
PCAT1 Supports Partial AR-V7 Function and Promotes Enzalutamide Resistance in Prostate Cancer.
Article in International journal of general medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Enzalutamide resistance (Enz-R) remains a major clinical challenge in advanced prostate cancer (PCa). Here, we identified resistance-associated long non-coding RNA (lncRNA) PCAT1 and investigated its functional relevance in Enz-R PCa. Methods: Public transcriptomic datasets, bioinformatic analyses, RNA immunoprecipitation (RIP), ChIP-qPCR, and in vitro and in vivo functional assays were used to evaluate the expression, function, and potential mechanism of PCAT1 in Enz-R PCa models. Results: PCAT1 was upregulated in Enz-R PCa models and was associated with adverse clinical features. PCAT1 knockdown inhibited the growth of C4-2 Enz-R cells and 22Rv1 cells and suppressed tumor growth in vivo. Mechanistically, PCAT1 was associated with AR/AR-V7 and supported selected AR-V7-associated downstream outputs without markedly altering AR-V7 protein expression. AR-V7 ChIP-qPCR further suggested that PCAT1 knockdown reduced AR-V7 enrichment at selected regulatory regions, including the KLK3 and PMEPA1 enhancers. In addition, high-dose androgen treatment reduced PCAT1 and AR-V7 expression in our experimental model. Conclusion: PCAT1 contributes to Enz-R PCa growth and may support selected AR-V7-associated transcriptional outputs. PCAT1 may represent a potential therapeutic vulnerability, and the relationship between high-dose androgen treatment, PCAT1 suppression, and AR-V7 signaling warrants further investigation.
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