CHIN-YUAN HSIEH2026-10-162026-10-162016-12-01Pure ID: 15191693Pure UUID: 61bbdb57-8eda-45eb-b443-2a135dff4e0810.1002/tox.22189https://www.scopus.com/pages/publications/84940205066https://scholars.csmu.edu.tw/handle/123456789/33226In 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.9enMitotic arrest induced in human DU145 prostate cancer cells in response to KHC-4 treatmentjournal article