Abstract
<p>Prostate cancer (PC) treatment with steroid synthesis inhibitor, abiraterone acetate (AA) provides substantial survival advantages in advanced PC therapy. Owing to AA's anti-proliferative efficacy, even in the absence of androgen receptor (AR), the molecular mode of action is suspected to be a result of simultaneously targeted cellular factors. The present study demonstrated a differentially regulated expression of proliferative lysophosphatidic acid receptor (LPAR) isoforms in androgen receptor AR-positive LNCaP cells incubated with AA. Since LPAR regulation in AR-negative PC-3 cells is unaffected, it could be assumed that AA’s anticancer activity on LPAR expression depends on AR signaling cascades.</p>
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