Abstract | BACKGROUND: METHODS: RESULTS: When combined with TRAIL, VEDT significantly augmented TRAIL-induced apoptosis of pancreatic cancer cells. VEDT decreased cellular FLICE inhibitory protein (c-FLIP) levels without consistently modulating the expression of decoy death receptors 1, 2, 3 or death receptors 4 and 5. Enforced expression of c-FLIP substantially attenuated VEDT/TRAIL-induced apoptosis. Thus, c-FLIP reduction plays an important part in mediating VEDT/TRAIL-induced apoptosis. Moreover, VEDT increased c-FLIP ubiquitination and degradation but did not affect its transcription, suggesting that VEDT decreases c-FLIP levels through promoting its degradation. Of note, degradation of c-FLIP and enhanced TRAIL-induced apoptosis in pancreatic cancer cells were observed only with the anticancer bioactive vitamin E compounds δ-, γ-, and β- tocotrienol but not with the anticancer inactive vitamin E compounds α- tocotrienol and α-, β-, γ-, and δ- tocopherol. CONCLUSIONS:
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Authors | Rony A Francois, Anying Zhang, Kazim Husain, Chen Wang, Sean Hutchinson, Michael Kongnyuy, Surinder K Batra, Domenico Coppola, Said M Sebti, Mokenge P Malafa |
Journal | Cancer cell international
(Cancer Cell Int)
Vol. 19
Pg. 189
( 2019)
ISSN: 1475-2867 [Print] England |
PMID | 31367187
(Publication Type: Journal Article)
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