APOC1 silencing inhibited cell proliferation and colony formation, arrested cell cycle progression, and enhanced apoptosis in DU145 prostate cancer cells.
Does APOC1 knockdown inhibit cell proliferation and enhance apoptosis in prostate cancer cells?
APOC1 exhibits procarcinogenic effects in prostate cancer cells, suggesting it may serve as a potential therapeutic target.
Here, we aimed to investigate the carcinogenic effects of apolipoprotein C1 (APOC1) in prostate cancer (PCa). APOC1 expression was evaluated in PCa and normal prostate specimens, and lentivirus-mediated RNA interference was used to knockdown APOC1 in DU145 cells. The effects of APOC1 silencing on cell proliferation, cell cycle arrest, and apoptosis were assessed. APOC1 expression was much higher in PCa tissues than in normal tissues. Moreover, APOC1 silencing inhibited cell proliferation and colony formation, arrested cell cycle progression, and enhanced apoptosis in DU145 cells. Additionally, APOC1 silencing decreased survivin, phospho-Rb, and p21 levels and increased cleaved caspase-3 expression. These data supported the procarcinogenic effects of APOC1 in the pathogenesis of PCa and suggested that targeting APOC1 may have applications in the treatment of PCa.
Su et al. (Wed,) conducted a other in Prostate cancer. APOC1 silencing via lentivirus-mediated RNA interference vs. Normal prostate specimens / control cells was evaluated on Cell proliferation, cell cycle arrest, and apoptosis. APOC1 silencing inhibited cell proliferation and colony formation, arrested cell cycle progression, and enhanced apoptosis in DU145 prostate cancer cells.