Key result
APOC1 knockdown increases DU145 prostate cancer cell apoptosis from ~6% to ~35%.
APOC1 knockdown inhibits prostate cancer cell proliferation and induces apoptosis in vitro, suggesting it may be a potential therapeutic target for prostate cancer.
APOC1 may represent a prostate cancer target; hypothesis-generating in vitro result requires in vivo validation before clinical exploration.
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.
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Su et al. (2018) studied Prostate cancer (n=324). APOC1 knockdown via shRNA vs. Negative control shRNA (shCon) was evaluated on Apoptosis rate in DU145 prostate cancer cells (p=<0.001). Knockdown of APOC1 expression in DU145 prostate cancer cells significantly inhibited cell proliferation, arrested the cell cycle, and increased apoptosis from 6.3% to up to 35.4%.
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