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ARSENIC TRIOXIDE DOWNREGULATES TELOMERASE ACTIVITY IN HL-60 CELLS

机译:三氧化二砷下调HL-60细胞端粒酶活性

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Objective: To evaluate whether arsenic trioxide (AS2O3) could downregulate human telomerase reverse transcriptase (hTERT) gene expression and telomerase activity during induction of apoptosis of HL-60 cells. Methods: Apoptosis was detected by morphological observation and flow cytomertric cell cycle analysis. The expression of hTERT at mRNA and protein levels was analyzed by reverse transcriptase polymerase chain reaction (RT-PCR) and immunofluorescence using fluoresce isothiocyanate (FITC) label, respectively. Telomerase activity was determined by polymerase chain reaction enzyme-linked immunoassay (PCR-ELISA). Results: Treatment of 2 μmol/L at As2O3 could induce apoptosis of HL-60 cells. hTERT was decreased at both mRNA and protein levels during apoptosis of HL-60 cells. Telomerase activity of HL-60 cells was significantly inhibited. Conclusion:It is suggested that telomerase activity of HL-60 cells might be specifically inhibited by AS2O3 through the downregulation of hTERT gene expression.
机译:目的:探讨三氧化二砷(AS2O3)在诱导HL-60细胞凋亡过程中是否下调人端粒酶逆转录酶(hTERT)基因表达和端粒酶活性。方法:通过形态学观察和流式细胞仪检测细胞凋亡。分别通过逆转录酶聚合酶链反应(RT-PCR)和使用异硫氰酸荧光素(FITC)标记的免疫荧光分析了hTERT在mRNA和蛋白水平上的表达。端粒酶活性通过聚合酶链反应酶联免疫法(PCR-ELISA)确定。结果:As2O3处理2μmol/ L可以诱导HL-60细胞凋亡。 HL-60细胞凋亡期间,hTERT在mRNA和蛋白水平均下降。 HL-60细胞的端粒酶活性被显着抑制。结论:AS2O3可能通过下调hTERT基因的表达来抑制HL-60细胞的端粒酶活性。

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