PUMA promotes apoptosis of pancreatic carcinoma BxPC-3 cells and the possible mechanism
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Abstract:
Objective:To investigate the effect of P53 upregulate modulator of apoptosis (PUMA) on the apoptosis of pancreatic carcinoma BxPC3 cells and the possible mechanism. Methods: BxPC3 cells were infected with recombinant adenovirus containing PUMA gene (AdPUMA) at 100 MOI for 096 h. Apoptosis of BxPC3 cells was examined by FCM. Expressions of PUMA, Bcl2, Bax, Cytochrome C and Caspase3 proteins in BxPC3 cells were detected by Western blotting. Bax expression in the cytoplasm and mitochondrion and Bax oligomer expression expression in BxPC3 cells were determined by Western blotting. Results:Apoptosis rates of BxPC3 cells were significantly increased with the time of AdPUMA infection, and peaked after 48 h. AdPUMA infection increased the expressions of PUMA, Cytochrome C and Caspase3 proteins in BxPC3 cells, and decreased the expression of Bcl2 protein. Apoptosis rate of BxPC3 cells after AdPUMA infection was correlated with PUMA expression. AdPUMA did not affect the expression of total Bax protein in BxPC3 cells, but Bax expression in cytoplasm was dramatically decreased after infection, and Bax expression in mitochondrion was markedly increased. Furthermore, AdPUMA infection induced Bax oligomerization in BxPC3 cells.Conclusion: PUMA can promote apoptosis of pancreatic carcinoma cells through mitochondrion pathway.
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Supported by the Scientific Research Foundation from Ministry of Health (No. WKJ200601010)