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Journal of Biochemistry Advance Access originally published online on May 31, 2008
Journal of Biochemistry 2008 144(3):357-362; doi:10.1093/jb/mvn074
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© 2008 The Japanese Biochemical Society

Valproic Acid Inhibits the Growth of Cervical Cancer both In Vitro and In Vivo

Siraj Sami1, Naseruddin Höti2, Han-Mei Xu1,*, Zilong Shen1 and Xiaofeng Huang3

1The Center of Biotechnology, College of Life Sciences and Technology, China Pharmaceutical University, Nanjing 210009, People's Republic of China; 2James Buchanan Brady Urological Institute, Johns Hopkins University School of Medicine, 600N. Wolfe Street, Baltimore, MD 21287-2101, USA; and 3Department of Oral Pathology, Nanjing Stomatological Hospital, Affiliated Medical School, Nanjing University, Nanjing 210093, People's Republic of China

*To whom correspondence should addressed. Tel: +86 25 8327 1007, Fax: +86 25 85438355, E-mail: xuhanmei{at}yahoo.com.cn

Received February 18, 2008; Accepted May 22, 2008


  Abstract

Valproic acid (VPA), a well-known anti-convulsant, is currently under extensive evaluation as an anti-cancer agent. It is known to exert its anti-cancer effect mainly by inhibiting the enzyme histone deacetylase I. In our study, we investigated the effects of VPA on cervical cancer both in vitro and in vivo cancer models. We examined the effects of acute VPA (0, 1.2, 2.4, 5.0 mM) treatment on cell proliferation in cervical cancer cell lines HeLa, SiHa and Ca Ski and histone acetylation, p21 and p53 gene expression in HeLa cell line. We also investigated the effect of chronic VPA administration in tumour xenograft growth studies. Our results show that with acute treatment, VPA can increase the expression of net histone H3 acetylation and up-regulate p21 expression with no effect on p53 expression. Chronic administration of VPA had a net cytostatic effect that resulted in a statistically significant reduction of tumour growth and improved survival advantages in tumour xenografts studies. Furthermore, we also demonstrated that VPA has a direct anti-angiogenic effect in tumour studies and could potentially be a promising candidate for further cervical cancer trails.

Key Words: angiogenesis, cervical cancer, p21, p53, valproic acid

Abbreviations: HDAC, histone deacetylase; HIF-1{alpha}, hypoxia-inducible factor 1{alpha}; HPV, human papilloma viruses; H3 Ac, histone 3 acetylation; VEGF, vascular endothelial growth factor; VPA, valproic acid


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