Tyrosine kinase inhibitor p15 gene in transfected K562 cells.docVIP

 PAGE \* MERGEFORMAT 24 Tyrosine kinase inhibitor p15 gene in transfected K562 cells Abstract This study investigated the tyrosine kinase inhibitor imatinib mesylate (imatinib) and the combined effects of p15 gene was cloned K562 cell proliferation, cell cycle and apoptosis such as in vitro. By RT  PCR amplification of p15 gene, gel purification of the recovered to connect to the T vector and sequenced to confirm the correct sequence to build after the p15  pcDNA3.1 vector, the p15  pcDNA3.1 empty vector, respectively, with liposome was transfected into p15 mutation K562 cells were screened by G418 resistant K562 cell line; detected by Western blot after transfection, the expression of P15 protein; Determination of cell survival using MTT; by flow cytometry cell cycle and apoptosis. The results showed that: From the control K562 cells amplified DNA fragments, in the first 174-180 sites 7 bp deletion, which confirmed that K562 cells in control parts of p15 gene mutations. P15 protein expression of exogenous p15  pcDNA3.1  K562 cell line growth rate significantly slower than the control K562 cell line; flow cytometry showed an increase in G0/G1 phase cells, S phase cells decreased; p15  pcDNA3.1  K562 cells with imatinib in combination significantly increased the apoptotic cell ratio, MTT assay showed cell viability was significantly decreased compared with control cells. Conclusion: The expression of P15 protein, combined with exogenous imatinib to inhibit K562 cell proliferation and apoptosis has a synergistic effect. Keywords: p15 gene tyrosine kinase inhibitor imatinib in K562 cells, Effect of Tyrosine  kinase Inhibitor on p15 Gene Transfected K562 Cells Abstract The objective of study was to investigate the combined effect of tyrosine  kinase inhibitor (imatinib) and p15 gene on the proliferation, cell cycle and apoptosis of chronic myeloid leukemia cell line K562. P15 gene was amplified from peripheral blood mononuclear