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http://dx.doi.org/10.5352/JLS.2015.25.11.1331

Anticarcinogenic Effect of S-allylcysteine (SAC)  

Kong, Il-Keun (Department of Animal Science, Division of Applied Life Science (BK21 plus), Gyeongsang National University)
Kim, Hyun Hee (Department of Animal Science, Division of Applied Life Science (BK21 plus), Gyeongsang National University)
Min, Gyesik (Department of Nursing, College of Life Science, Gyeongnam National University of Science & Technology)
Publication Information
Journal of Life Science / v.25, no.11, 2015 , pp. 1331-1337 More about this Journal
Abstract
S-allylcysteine (SAC) is an aged garlic derived water soluble organosulfur compound and has been suggested to have anticarcinogenic activity against diverse types of cancer cells. This review summarizes the cellular signaling pathways and molecular mechanisms whereby SAC exerts its effects on cellular proliferation, apoptosis, cell cycle progression and metastasis based on the results from both in vitro and in vivo studies. SAC activates proapoptotic proteins including Bax and caspase-3, but suppresses antiapoptotic Bcl-2 family proteins to bring about cancer cell death through mitochondria-mediated intrinsic pathway. SAC also inhibits cellular proliferation by inducing cell cycle arrest in which SAC reduces expression and activation of NF-κB, cyclins, Cdks, PCNA and c-Jun, but elevates expression of cell cycle inhibitor proteins p16 and p21 through suppression of both PI3K/Akt/mTOR and MAPK/ERK signaling pathways. And, SAC inhibits invasion and metastasis of cancer cells by inducing suppression of both angiogenesis and epithelial-mesenchymal transition (EMT) through decreased cyclooxygenase (COX)-2 expression and increased E-cadherin expression which were then caused by suppression of inhibitory transcription factors Id-1 and SLUG from SAC-mediated inactivation of both MAPK/ERK and PI3K/Akt/mTOR/NF-κB signaling pathways. Furthermore, SAC prevents toxic compound-induced carcinogenesis by inducing antioxidant enzymes such as glutathione-s-transferase (GST). Thus, SAC can be considered as a potential chemotherapeutic agent for the prevention and treatment of cancer.
Keywords
Apoptosis; cell cycle; cell proliferation; epithelial-mesenchymal transition (EMT); S-allylcysteine (SAC);
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