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Effect of DAPK overexpression on biological behaviors and caspase-3 expression in HL-60 cells / 南方医科大学学报
Journal of Southern Medical University ; (12): 729-732, 2016.
Article in Chinese | WPRIM | ID: wpr-263971
ABSTRACT
<p><b>OBJECTIVE</b>To explore the effect of DAPK overexpression on the biological behaviors and caspase-3 expression in HL-60 cells.</p><p><b>METHODS</b>The expression of DAPK mRNA was detected by RT-PCR leukemia cell lines K562, Molt4, U937, and HL-60 cells. HL-60 cells were transfected by a eukaryotic expression vector pReceiver-M29-DAPK via LipofectamineTM 2000, and the impact of DAPK overexpression on cell apoptosis, cell cycle, cell differentiation and caspase-3 expression were analyzed.</p><p><b>RESULTS</b>DAPK mRNA expression was positive in K562, Molt4 and U937 cells but negative in HL-60 cells. Significantly increased cell apoptosis was observed in pReceiver-M29-DAPK-transfected HL-60 cells by flow cytometry and Hoechst33342 staining. The cell cycle distribution and differentiation showed no significant changes after the transfection. The expression of caspase-3 was significantly increased in the cells after transfection.</p><p><b>CONCLUSION</b>DAPK gene overexpression promotes apoptosis of HL-60 cells without affecting the cell cycle and differentiation. Caspase-3 may be involved in the regulation of cell apoptosis.</p>
Subject(s)
Full text: Available Index: WPRIM (Western Pacific) Main subject: RNA, Messenger / Transfection / Cell Cycle / Cell Differentiation / Apoptosis / HL-60 Cells / U937 Cells / Cell Line, Tumor / Caspase 3 / Death-Associated Protein Kinases Limits: Humans Language: Chinese Journal: Journal of Southern Medical University Year: 2016 Type: Article

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Full text: Available Index: WPRIM (Western Pacific) Main subject: RNA, Messenger / Transfection / Cell Cycle / Cell Differentiation / Apoptosis / HL-60 Cells / U937 Cells / Cell Line, Tumor / Caspase 3 / Death-Associated Protein Kinases Limits: Humans Language: Chinese Journal: Journal of Southern Medical University Year: 2016 Type: Article