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Approximately 61,000 statements.
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Copyright (c) 2011-2012, Selventa. All rights reserved.
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Treatment of OV2008 cells with neither TNF alpha (20 ng/ml) nor CHX (10 microg/ml) alone had any apparent effects on the processing of intracellular proteins. However, in the presence of CHX, TNF alpha induced cleavage of the caspases and XIAP, a phenomenon suppressed by the presence of caspase inhibitors [ZVAD (50 microM) and DEVD (20 microM). Moreover, TNF alpha alone had no effect on XIAP content in OV2008 cells. These observations suggested that, the presence but not absence of the protein synthesis inhibitor, TNF alpha is capable of activating caspase-8 and -3 and inducing XIAP cleavage during the induction of apoptosis, while the putative survival factor is likely acting upstream of caspase-8. In addition TNF alpha induced the expression of FLIP(S) but not of FLIP(L) in OV2008 cells in the concentration- and time-dependent manner, lowering FLIP(S) levels by antisense expression facilitated the proapoptotic action of the cytokine. This study demonstrated that TNFalpha up-regulates FLIP(S) expression, which is mediated by the activation of nuclear factor kappaB and the induction of FLIP(S) expression by TNFalpha might contribute to the resistance of ovarian epithelial cancer cells to the proapoptotic action of the cytokine.
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Selventa
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2014-07-03T14:30:09.518+02:00
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