ArticleThe world journal of men's health2026
Inhibition of PREX1 Reverses Enzalutamide Resistance in Castration-Resistant Prostate Cancer.
Article in The world journal of men's health, 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
purposeCastration-resistant prostate cancer (CRPC) often progresses despite initial responses to enzalutamide owing to the development of resistance. Our study explored the mechanisms underlying resistance in enzalutamide-resistant prostate cancer cell lines, along with the role of phosphatidylinositol-3,4,5-trisphosphate-dependent Rac exchanger 1 (PREX1) in CRPC resistance. MATERIALS AND
methodsThe sequencing of total RNA was performed to analyze the microarray gene expression profiles. In our colony formation assay, 1,000 cells per well were seeded into six-well plates to evaluate clonogenic survival. Phosphoprotein profiling was conducted to assess specific signaling pathways and estimate cell proliferation rates. Protein expression was analyzed by western blotting, and Rac GTPase activity was measured to evaluate the cellular responses to enzalutamide. Cell invasion was examined using Transwell migration assays. An
resultsRNA sequencing revealed activation of the cancer migration pathway in enzalutamide-resistant prostate cancer cells with significant upregulation of PREX1. PREX1 knockdown reduced the proliferation and colony formation rates of resistant cell lines. Mechanistically, PREX1 suppression inhibited both epidermal growth factor receptor and its downstream signaling pathways, including signal transducers and activators of transcription 5, thereby reducing cell migration and epithelial-mesenchymal transition, independent of Rac activation.
conclusionsThis study provides compelling evidence on the pivotal role of PREX1 in mediating enzalutamide resistance in CRPC. Our findings suggest that PREX1 is a promising therapeutic target that may modulate treatment efficacy and drug resistance in CRPC.
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