The Affect Of NVO-BEZ235through PI3K Signaling Pathway On Jurkat Cell Cycle And Apoptosis Of T-cell Acute Lymphoblastic Leukemia

Objective: To investigate the effects of PI3K inhibitors(NVP-BEZ235)onproliferation、apoptosis and the protein (Akt、p70s6k)’s phosphorylation ofPI3K-AKT-mTOR signaling pathway in human T-cell Acute LymphoblasticLeukemia Jurkat T-cell,so as to provides the experimental basis for improvingclinical treatment of T-cell Acute Lymphoblastic Leukemia.Methods: Assessed proliferation of human T-cell Acute LymphoblasticLeukemia Jurkat T-cell with MTT after it dealt with different doses and timepoints by NVP-BEZ235, on this basis, Using flow cytometry to detect thechange of cell cycle and apoptosis rate of Jurkat T-cell which dealt withNVP-BEZ235, testing PI3K signaling pathway protein(Akt、p70s6k)’sphosphorylation whether reduced with Western blot.Results: After processed by different concentration NVP-BEZ235indifferent time, NVP-BEZ235can inhibit the colony formation. proliferation andpromote apoptosis of Jurkat T cell in different degree, the test results of flowcytometry instrument showed that different concentrations of NVP-BEZ235canpromote cell apoptosis, and the concentration in accordance with patience; Thecell cycle results showed that NVP-BEZ235block Jurkat T cells in G1/G0phase.By Western blotting methods showed that protein (Akt, p70s6k)‘sphosphorylation of Jurkat T cells reduced significantly by NVP-BEZ235.Conclusion: The activation of PI3K signaling pathways exist in Acute Tlymphocyte leukemia，PI3K/mTOR double inhibitors NVP-BEZ235fortargeting therapy of acute T lymphocyte leukemia to provide experimental basis.