XXXX induces apoptosis of human @entity995 cells via activation of @entity4012 .

@entity4404 @entity12982 @entity1191 @entity4012 @entity9800 @entity995
PURPOSE: The purpose of this study was to investigate the pro-apoptotic effect of @entity9800 ( @entity1191 ) on Y79 @entity995 cells and the role of Forkhead box, class O ( @entity4012 ) in @entity1191 -induced apoptosis. METHODS: @entity1191 -induced apoptosis was determined by flow cytometry with @entity4404 -FITC positive cells and Western blot of @entity12982 expression, respectively. The expressions of @entity4012 were detected by Western blot. The transcriptional activity of @entity4012 was determined by luciferase reporter assay. siRNAs specifically inhibiting @entity4012 were used, and flow cytometry and Western blot were executed to test the role of @entity4012 in @entity1191 -induced apoptosis. RESULTS: @entity1191 was extremely effective in inducing apoptosis of Y79 @entity995 cells. @entity4012 was highly expressed in Y79 cells. @entity1191 not only elevated the @entity4012 dephosphorylation level but also promoted its transcriptional activity, suggesting that the activation of @entity4012 was, at least in part, triggered by @entity1191 . The decreased @entity4404 positive cells and less @entity12982 cleavage demonstrated that siRNAs-mediated inhibition of @entity4012 significantly abrogated @entity1191 -induced apoptosis, indicating that @entity4012 plays an important role in @entity1191 -induced apoptosis. Moreover, the expression of Bim was also elevated with the treatment of @entity1191 , which is in accordance with the activation of @entity4012 . CONCLUSIONS: Our study provides the evidence that a high level of endogenous @entity4012 expression in @entity995 cells contributes, at least in part, to @entity1191 -induced apoptosis, which may help broad application of @entity1191 in @entity995 therapy in the future.
