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http://dx.doi.org/10.5352/JLS.2017.27.2.164

S-allylcysteine-mediated Activation of Caspases and Inactivation of PARP to Inhibit Proliferation of HeLa  

Kim, Hyun Hee (Department of Animal Science, Division of Applied Life Science (BK21 plus), Gyeongsang National University)
Kong, Il-Keun (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.27, no.2, 2017 , pp. 164-171 More about this Journal
Abstract
Our previous study suggested that S-allylcysteine (SAC) inhibits the proliferation of the human cervical cancer cell line, HeLa, at least in part through the induction of apoptosis and cell cycle arrest. To further analyze the specific molecular mechanism(s) by which SAC mediates its antiproliferative effects, this study examined the role of SAC in regulating the protein expression of initiator caspase (caspase-9), effector caspases (caspase-3 and caspase-7), and poly-ADP-ribose polymerase (PARP) in HeLa. Western blot analysis showed that when cells were treated with 50 mM SAC for 48 hr, the expression of procaspase-3, -7, and -9 and PARP was reduced by 94%, 38%, 95%, and 64%, respectively, as compared to the untreated control. In contrast, the expression of caspase-3, -7, and -9 and cleaved-PARP was markedly increased by SAC treatment. The SAC-mediated changes in the expression of these proteins were correlated with the concomitant inhibition of cellular proliferation by SAC. The cell proliferation assay showed that HeLa treatment with more than 20 mM SAC for 6-48 hr resulted in both concentration- and time-dependent inhibition of cellular proliferation. These results indicate that the SAC-induced antiproliferative effect in HeLa may be mediated at least in part through the activation of caspase-9, followed by the activation of caspase-3 and caspase-7 as well as the inactivation of PARP, thus leading to cellular apoptosis.
Keywords
Apoptosis; caspase; cell proliferation; poly-ADP-ribose polymerase (PARP); S-allylcysteine (SAC);
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