Journal
JOURNAL OF CELLULAR BIOCHEMISTRY
Volume 113, Issue 9, Pages 2835-2844Publisher
WILEY
DOI: 10.1002/jcb.24158
Keywords
SULFURETIN; Rhus verniciflua; APOPTOSIS; Fas; Caspase-8; Bcl-2
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Funding
- Ministry of Education, Science and Technology (National Research Foundation of Korea (NRF)) [2009-0088135]
- National Research Foundation of Korea [2009-0088135] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
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Sulfuretin, a flavonoid isolated from heartwood of Rhus verniciflua, has been reported to have anti-cancer activities but the underlying molecular mechanism was not clear. In this study, sulfuretin induced apoptosis by activating caspases-8, -9, and -3 as well as cleavage of poly(ADP-ribose) polymerase. Furthermore, treatment with sulfuretin caused mitochondrial dysfunctions, including the loss of mitochondrial membrane potential (??m), the release of cytochrome c to the cytosol, and the translocations of Bax and tBid. Sulfuretin also activated the extrinsic apoptosis pathway, that is, it increased the expressions of Fas and FasL, the activation of caspase-8, and the cleavage of Bid. Furthermore, blocking the FasLFas interaction with NOK-1 monoclonal antibody prevented the sulfuretin-induced apoptosis. The therapeutical effect of sulfuretin in leukemia is due to its potent apoptotic activity through the extrinsic pathway driven by a Fas-mediated caspase-8-dependent pathway. J. Cell. Biochem. 113: 28352844, 2012. (C) 2012 Wiley Periodicals, Inc.
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