Molecular Mechanism of PTEN Gene Influencing K562 Cell Cycle

【Objective】To investigate the effect of tumor suppressor wild type PTEN gene (phosphatase and tensin hemology deleted on chromosome ten gene) on the cell apoptosis and cell cycle of human chronic myeloid leukemia (CML) cell line K562 in vitro. 【Methods】 The recombination of wild type PTEN gene and adenovirus with green fluorescent protein (GFP) (Ad-PTEN- GFP) and control vector adenovirus (Ad-GFP) were transfected into K562 cell lines. The inhibitory rate of cell proliferation was detected by MTT assay and the transfection efficiency of Ad-PTEN-GFP, apoptosis rate and cell cycle were assessed by flow cytometry (FCM). The transcription changes of PTEN, Cyclin D1, Cyclin D2, CDK4, and P27Kip1 mRNA were measured by fluorescent quantitative PCR (FQ-PCR), and their protein levels were measured by Western blotting. 【Results】 Compared with transfected Ad-GFP, the highest apoptosis rate was 30% after transfected with Ad-PTEN-GFP in K562 cell lines. The ratio of G0/ G1 phase cells increased from 54.9% to 78.5% and reduced from 30.2% to 13.6% in G2/ M phase cells. Protein expression levels of Cyclin D1, Cyclin D2, CDK4 Mrna, and Cyclin D1 down-regulated and P27Kip1 mRNA and protein expression up-regulated after the cells transfected with PTEN gene. 【Conclusion】 Over expression of PTEN gene can promote the apoptosis of K562 cells in vitro and block cell cycle progression at G0 / G1 phase by down-regulating Cyclin D1, Cyclin D2, CDK4 expression and up- regulating P27 Kip1 expression.