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Apolipoprotein C1 promotes prostate cancer cell proliferation in vitro
Author(s) -
Su Weipeng,
Sun Lina,
Yang Shunliang,
Zhao Hu,
Zeng Tengyue,
Wu Weizhen,
Wang Dong
Publication year - 2018
Publication title -
journal of biochemical and molecular toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.526
H-Index - 58
eISSN - 1099-0461
pISSN - 1095-6670
DOI - 10.1002/jbt.22158
Subject(s) - du145 , gene silencing , gene knockdown , cancer research , cell cycle , cell growth , survivin , prostate cancer , apoptosis , rna interference , chemistry , cell cycle checkpoint , cell , biology , microbiology and biotechnology , cancer , lncap , rna , biochemistry , genetics , gene
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.