Carcinogenesis Advance Access originally published online on May 4, 2006
Carcinogenesis 2006 27(11):2180-2189; doi:10.1093/carcin/bgl054
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A novel anticancer effect of garlic derivatives: inhibition of cancer cell invasion through restoration of E-cadherin expression
Cancer Biology Group, Department of Anatomy, Faculty of Medicine, The University of Hong Kong Hong Kong, China
*To whom correspondence should be addressed at: Department of Anatomy, The University of Hong Kong, 1/F, Faculty of Medicine Building, 21 Sassoon Road, Hong Kong, China. Tel: +852 2819 2867; Fax: +852 2817 0857; Email: TUxhwang{at}hkucc.hku.hkUT and Uycwong{at}hkucc.hku.hk
Metastatic cancer is one of the main causes of cancer-related death since they rarely respond to available treatments. Recently, certain compounds isolated from the dietary supplement, garlic, have shown anti-proliferation effect on cancer cells. The aim of this study was to investigate whether certain garlic derivatives had any effect on the potentially invasive androgen-independent prostate cancer (PCa) cells. Using colony-forming, wound-closure as well as matrigel-invasion assays, we found that two main water-soluble constituents of the garlic, S-allylcysteine (SAC) and S-allylmercaptocysteine (SAMC), were able to suppress PCa cell proliferation and invasive abilities. This inhibitory effect was associated with induction of mesenchymal to epithelial transition. Most importantly, the SAC and SAMC treatment led to restoration of E-cadherin expression at transcription and protein levels. In contrast, the expression of E-cadherin repressor, Snail, was reduced in the SAC- and SAMC-treated cells. Furthermore, examination of cell lines from other types of cancer (ovarian, nasopharyngeal and esophageal carcinomas) also confirmed that the effect of SAC and SAMC on activation of E-cadherin might be a general effect on human cancer cells. Our results demonstrate a novel anticancer effect of garlic and suggest that certain garlic-derived compounds may be potential agents for suppression of invasive growth through restoration of E-cadherin expression in cancer cells.
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