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Hispolon Induces Apoptosis and Cell Cycle Arrest of Human Hepatocellular Carcinoma Hep3B Cells by Modulating ERK Phosphorylation

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    Hispolon Induces Apoptosis and Cell Cycle Arrest of Human Hepatocellular Carcinoma Hep3B Cells by Modulating ERK Phosphorylation
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    † School of Chinese Pharmaceutical Sciences and Chinese Medicine Resources, College of Pharmacy, China Medical University, Taichung, Taiwan
    § Department of Health and Nutrition Biotechnology, Asia University, Taichung 413, Taiwan
    # Department of Food Science and Biotechnology, National Chung Hsing University, Kuo-Kuang Road, Taichung, Taiwan
    ⊥ Institute of Nutrition, China Medical University, Taichung, Taiwan
    Postal address: Department of Food Science and Biotechnology, National Chung Hsing University, 250 Kuo-Kuang Road, Taichung 402, Taiwan. Phone: +886 4 2281 2363. Fax: +886 4 2287 6211. E-mail: [email protected]
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    Journal of Agricultural and Food Chemistry

    Cite this: J. Agric. Food Chem. 2011, 59, 13, 7104–7113
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    https://doi.org/10.1021/jf201289e
    Published June 1, 2011
    Copyright © 2011 American Chemical Society
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    Abstract

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    Hispolon is an active phenolic compound of Phellinus igniarius, a mushroom that has recently been shown to have antioxidant, anti-inflammatory, and anticancer activities. This study investigated the antiproliferative effect of hispolon on human hepatocellular carcinoma Hep3B cells by using the MTT assay, DNA fragmentation, DAPI (4,6-diamidino-2-phenylindole dihydrochloride) staining, and flow cytometric analyses. Hispolon inhibited cellular growth of Hep3B cells in a time-dependent and dose-dependent manner, through the induction of cell cycle arrest at S phase measured using flow cytometric analysis and apoptotic cell death, as demonstrated by DNA laddering. Hispolon-induced S-phase arrest was associated with a marked decrease in the protein expression of cyclins A and E and cyclin-dependent kinase (CDK) 2, with concomitant induction of p21waf1/Cip1 and p27Kip1. Exposure of Hep3B cells to hispolon resulted in apoptosis as evidenced by caspase activation, PARP cleavage, and DNA fragmentation. Hispolon treatment also activated JNK, p38 MAPK, and ERK expression. Inhibitors of ERK (PB98095), but not those of JNK (SP600125) and p38 MAPK (SB203580), suppressed hispolon-induced S-phase arrest and apoptosis in Hep3B cells. These findings establish a mechanistic link between the MAPK pathway and hispolon-induced cell cycle arrest and apoptosis in Hep3B cells.

    Copyright © 2011 American Chemical Society

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    Structure and experimental data of hispolon. This material is available free of charge via the Internet at http://pubs.acs.org.

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    This article is cited by 52 publications.

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    Journal of Agricultural and Food Chemistry

    Cite this: J. Agric. Food Chem. 2011, 59, 13, 7104–7113
    Click to copy citationCitation copied!
    https://doi.org/10.1021/jf201289e
    Published June 1, 2011
    Copyright © 2011 American Chemical Society
    Request reuse permissions

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