Prostate cancer (PRAD) represents a significant health burden for men globally. By integrating publicly accessible datasets with immunohistochemistry, this investigation found that ACTC1 expression is markedly elevated in PRAD. In vitro experiments demonstrated that forced overexpression of ACTC1 stimulated cellular proliferation and migratory capacity, whereas its silencing inhibited these aggressive traits. These observations were corroborated in vivo, where xenograft models revealed that ACTC1 accelerated tumor expansion. Comprehensive transcriptomic profiling and pathway enrichment analyses indicated that ACTC1 modulates immune and inflammatory cascades, with BMP4 emerging as a critical downstream mediator. Notably, ectopic expression of BMP4 reversed the suppressive effects of ACTC1 depletion on cell growth and movement, establishing that ACTC1 exerts its pro-tumorigenic effects primarily via BMP4 signaling. Collectively, these data position ACTC1 as a novel oncogenic factor in prostate cancer progression and nominate the ACTC1–BMP4 signaling axis as a promising therapeutic target.
