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首页|miRNA-196b过表达对K562细胞增殖、凋亡及Survivin、Cox-2表达的影响

miRNA-196b过表达对K562细胞增殖、凋亡及Survivin、Cox-2表达的影响

Effects of miRNA-196b overexpression on Proliferation, Apoptosis and Survivin,Cox-2 Expression of K562 Cells

中文摘要英文摘要

目的:探讨miRNA-196b过表达对K562细胞增殖、凋亡及Cox-2、Survivin基因表达的影响。方法:实验分为miRNA-196b组、siRNA-ABL组、伊马替尼(IM)组与K562组,采用CCK-8法检测细胞增殖;采用Annexin V-PE检测细胞凋亡;采用实时荧光定量PCR法检测Cox-2、Survivin、基因的表达情况。结果:miRNA-196b过表达可以明显抑制K562细胞增殖;miRNA-196b组细胞凋亡率显著高于K562组和siRNA-ABL组,但低于伊马替尼组(P<0.05);miRNA-196b组中Survivin基因显著低表达(P<0.05)Cox2基因中无明显变化(P>0.05)。结论:miRNA-196b对K562细胞的增殖抑制和诱导凋亡有显著作用;miRNA-196b过表达可下调Survivin基因的表达,为miRNA-196b作为慢性粒细胞性白血病的治疗靶点提供了一定依据。?????

o investigate the effects of miRNA-196b overexpression on proliferation, apoptosis and Cox-2,survivin genes expression of K562 cells. Methods Four groups including miRNA-196b, siRNA-ABL, Imatinib(IM) and K562 control group were set up in this study. The cell proliferation and apoptosis were measured by CCK-8 assay and Annexin V-FITC/PI, respectively. The expression of Cox-2 and survivin genes at the mRNA level was detected by RT-qPCR. Results The proliferation of K562 cells could be significantly inhibited by miRNA-196b overexpression; Compared of the four groups of apoptosis rate, miRNA-196b group significantly higher than K562 and siRNA-ABL groups, but less than imatinib group (P < 0.05). The expression of survivin gene in miRNA-196b was donwregulated(P < 0.05),but the expression of cox-2 gene in miRNA-196b group had no significant difference(P>0.05).Conclusion The miRNA - 196b plays an important role in K562 cells proliferation inhibition and apoptosis;Overexpression of miRNA-196b can down-regulate surviving gene expression, provide some basis for miRNA-196b as a therapeutic target for chronic myelogenous leukemia.

尹虹、宋艳斌、陈滨、马文丽、郑文岭、刘玥

基础医学肿瘤学分子生物学

miRNA-196bsiRNA-ABL伊马替尼K562细胞细胞增殖细胞凋亡

miRNA-196b siRNA-ABLImatinib K562 cells cell Proliferation cell Apoptosis

尹虹,宋艳斌,陈滨,马文丽,郑文岭,刘玥.miRNA-196b过表达对K562细胞增殖、凋亡及Survivin、Cox-2表达的影响[EB/OL].(2013-01-25)[2025-08-02].http://www.paper.edu.cn/releasepaper/content/201301-1048.点此复制

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