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pubmed-article:19360359pubmed:abstractTextRecent studies establish a critical role of selenium in cancer prevention in vitro and in vivo. Selenium may sensitize TRAIL-mediated apoptosis in human renal cancer cells and increase therapeutic efficacy. In this study, we demonstrate that concomitant administration of TRAIL and Se-methylselenocysteine (Se-MSC) produces synergistic effects on the induction of apoptosis in Caki cells. Se-MSC rapidly and specifically down-regulates expression of the Bcl-2 at transcriptional level. The forced expression of Bcl-2 attenuated Se-MSC plus TRAIL-mediated apoptosis, suggesting that the lessened Bcl-2 expression caused by Se-MSC treatment is critical to the increased sensitivity to TRAIL in renal cancer cells. In addition, we demonstrate that the synergistic effects of Se-MSC and TRAIL result from the activation of the caspase-dependent pathways. Co-administration of HA14-1, a small molecule Bcl-2 inhibitor and TRAIL increased apoptosis in Caki cells. Taken together, Se-MSC-mediated down-regulation of Bcl-2 is able to sensitize Caki cells for TRAIL-induced apoptosis. Thus, selenium-based dietary compounds may help to overcome resistance to TRAIL-mediated apoptosis in renal cancer cells.lld:pubmed
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pubmed-article:19360359pubmed:authorpubmed-author:KwonTaeg...lld:pubmed
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pubmed-article:19360359pubmed:articleTitleSe-methylselenocysteine sensitized TRAIL-mediated apoptosis via down-regulation of Bcl-2 expression.lld:pubmed
pubmed-article:19360359pubmed:affiliationDepartment of Immunology and Chronic Disease Research Center and Institute for Medical Science, School of Medicine, Keimyung University, Jung-Gu, Taegu 700-712, Korea.lld:pubmed
pubmed-article:19360359pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:19360359pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed