alexa Diallyl Disulfide Increases Histone Acetylation and P21
ISSN: 2167-0501

Biochemistry & Pharmacology: Open Access
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Research Article

Diallyl Disulfide Increases Histone Acetylation and P21WAF1 Expression in Human Gastric Cancer Cells In vivo and In vitro

Bo Su1,2, Shu Lin Xiang1, Jian Su1,3, Hai Ling Tang1, Qiang Jin Liao1, Yu Juan Zhou1 and Su Qi1*
1Key Laboratory of Cancer Cellular and Molecular Pathology of Hunan Provincial University, Cancer Research Institute, University of South China, Hengyang, 421001 Hunan, P.R. China
2Division of Pharmacoproteomics, Institute of Pharmacy and Pharmacology, University of South China, Hengyang 421001, Hunan, P.R. China
3Department of Pathology, Second Affiliated Hospital, University of South China, Hengyang, 421001 Hunan, P.R. China
These authors contributed equally to this work.
Corresponding Author : Su Qi
Key Laboratory of Cancer Cellular and Molecular Pathology of Hunan Provincial University, Cancer Research Institute
University of South China, Hengyang, 421001 Hunan, P.R. China
Tel: +86-0734-8281547
Fax: +86-0734-8281547
E-mail: [email protected]
Received September 19, 2012; Accepted November 17, 2012; Published November 20, 2012
Citation: Su B, Xiang SL, Su J, Tang HL, Liao QJ, et al. (2012) Diallyl Disulfide Increases Histone Acetylation and P21WAF1 Expression in Human Gastric Cancer Cells In vivo and In vitro. Biochem Pharmacol 1:106. doi:10.4172/2167-0501.1000106
Copyright: © 2012 Su B, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited
 

Abstract

Diallyl disulfide (DADS) exerts numerous anticancer effects, involving multiple molecular mechanisms. In particular, DADS has been revealed as a potential inhibitor attenuating histone deacetylase (HDAC) activity, which could aid cancer prevention and therapy by inducing histone hyperacetylation and consequently reactivating epigenetically silenced tumor suppressor genes involved in cancer initiation and progression. In an in vitro study, we demonstrated that DADS increased histones H3 and H4 acetylation in human gastric cancer MGC803 cells in a time-dependent fashion, accompanied by increased p21WAF1 protein levels, which was consistent with G2/M phase cell cycle arrest. DADS
also demonstrated dose-dependent antitumor effects in MGC803-xenografted nude mice in vivo, resulting in tumor cells growth inhibition and G2/M phase arrest. Acetylated histones H3 and H4 were up-regulated by administration of DADS in association with elevated p21WAF1 protein expression. There was no evidence of gross toxicity associated with DADS treatment. DADS also preferentially enhanced acetylation of histone H3 relative to histone H4 both in vivo and in vitro. In addition, characteristic features of cell differentiation were observed in xenografted tumor cells. These results suggest that DADS can cause cell cycle arrest and inhibit cell proliferation by inducing hyperacetylation of histones
H3 and H4 and increasing p21WAF1 expression in MGC803 cells, which may partly account for its antitumor effects in gastric cancer. These results indicate that DADS may be useful for gastric cancer prevention, and may

 

have important implications for epigenetic therapy by virtue of its ability to modulate histone acetylation.

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