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Mitotic arrest induced in human DU145 prostate cancer cells in response to KHC‐4 treatment

Shen, Cheng‐Huang

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.

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Mitotic arrest induced in human DU145 prostate cancer cells in response to KHC‐4 treatment

Shen, Cheng‐Huang

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.

Mitotic arrest induced in human DU145 prostate cancer cells in response to KHC‐4 treatment

Shen, Cheng‐Huang

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.

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Title:

Mitotic arrest induced in human DU145 prostate cancer cells in response to KHC‐4 treatment

Contributors:

Shen, Cheng‐Huang (author) / Lin, Tien‐Huang / Hsieh, You‐Liang / Shen, Chia‐Yao / Kuo, Sheng‐Chu / Wu, Hsi‐Chin / Chien, Wen‐Shin / Hsieh, Dennis Jine‐Yuan / Wen, Su‐Ying / Ting, Wei‐Jen

Published in:

Environmental toxicology ; 31

Publication date:

2016

ISSN:

DOI:

https://doi.org/10.1002/tox.22189

Type of media:

Article (Journal)

Type of material:

Print

Language:

English

Keywords:

Umwelttoxikologie , Zeitschrift

Classification:

BKL: 43.00 Umweltforschung, Umweltschutz: Allgemeines / 43.00

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