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- W1973485395 abstract "The oncoprotein HER-2/neu is a prosurvival factor, and its overexpression has been correlated with poor prognosis in patients with breast cancer. We report that HER-2 is a new substrate for caspase-8 and that tumor necrosis factor alpha (TNF-alpha) stimulation leads to an early caspase-8-dependent HER-2 cleavage in MCF7 A/Z breast adenocarcinoma cells defective for nuclear factor kappaB (NFkappaB) activation. We show that the antiapoptotic transcription factor NFkappaB counteracts this cleavage through induction of the caspase-8 inhibitor c-FLIP. Our results also demonstrate that this HER-2 cleavage contributes to the TNF-alpha-induced apoptosis pathway because ectopic expression of an uncleavable HER-2 protects NFkappaB-defective cells against TNF-alpha-mediated cell death. Therefore, we propose an original model in which NFkappaB exerts a new antiapoptotic function by counteracting TNF-alpha-triggered cleavage of the HER-2 survival factor." @default.
- W1973485395 created "2016-06-24" @default.
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- W1973485395 date "2004-04-15" @default.
- W1973485395 modified "2023-10-13" @default.
- W1973485395 title "Caspase-8-Dependent HER-2 Cleavage in Response to Tumor Necrosis Factor α Stimulation Is Counteracted by Nuclear Factor κB through c-FLIP-L Expression" @default.
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- W1973485395 doi "https://doi.org/10.1158/0008-5472.can-03-2914" @default.
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