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Mitotic arrest induced in human DU 145 prostate cancer cells in response to KHC ‐4 treatment
Author(s) -
Shen ChengHuang,
Lin TienHuang,
Hsieh YouLiang,
Shen ChiaYao,
Kuo ShengChu,
Wu HsiChin,
Chien WenShin,
Hsieh Dennis JineYuan,
Wen SuYing,
Ting WeiJen,
Yao ChunHsu,
Huang ChihYang
Publication year - 2016
Publication title -
environmental toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.813
H-Index - 77
eISSN - 1522-7278
pISSN - 1520-4081
DOI - 10.1002/tox.22189
Subject(s) - du145 , prostate cancer , cell cycle , cancer research , mitosis , cyclin dependent kinase 1 , cell cycle checkpoint , population , cell growth , biology , chemistry , cell , microbiology and biotechnology , cancer , medicine , biochemistry , lncap , environmental health
In this study, the antitumor activity of KHC‐4 was analyzed using human prostate cancer (CaP) cells and the underlining anticancer mechanisms of KHC‐4 were identified. KHC‐4 inhibited cell proliferation and induced cytotoxicity in the castration‐resistant CaP DU145 cell line. The most effective concentration of KHC‐4 was 0.1 μM. Cell cycle analysis demonstrated that KHC‐4 treatment caused G2/M arrest and a subsequent increase in the sub‐G1 population. Furthermore, KHC‐4 is up‐regulated p21, p27, and p53 in a time‐ and concentration‐dependent manner. The exposure of cells to KHC‐4 induced Cdk1/cyclin B1 complex activity, which led to cell cycle arrest. Moreover, KHC‐4 inhibited the activities of MMP‐2 and MMP‐9 to inhibit tumor cell metastasis. © 2015 Wiley Periodicals, Inc. Environ Toxicol 31: 1879–1887, 2016.