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作 者:张诗蒙[1] 刘非 尹小毛[1] 郑磊[1] 王前[1]
机构地区:[1]南方医科大学南方医院检验科,广州市510515 [2]广州市妇女儿童医疗中心检验部,510623
出 处:《实用医学杂志》2014年第8期1182-1184,共3页The Journal of Practical Medicine
基 金:国家自然科学基金(编号:81371901);教育部博士点基金(编号:20134433110010)
摘 要:目的:通过体外实验研究过表达miR-27b对乳腺癌细胞系MCF-7增殖方面的影响,并探讨miR-27b的作用机制。方法:通过脂质体介导,将miR-27b mimics转染入MCF-7细胞,用荧光定量PCR检测细胞miR-27b的表达,用Western Blot检测PPARγ与NHE1的表达情况,再通过CCK8实验观察细胞增殖能力的改变。结果:MCF-7转染miR-27b mimics后,miR-27b的表达明显上调(P<0.05)。在蛋白水平,过表达miR-27b后,PPARγ的表达明显下调,而NHE1的表达明显上调。CCK8结果显示过表达miR-27b,细胞增殖作用增强。结论:miR-27b可抑制MCF-7细胞中靶基因PPARγ的表达,上调NHE1的表达水平,并且促进细胞增殖。Objective MiR-27b could promote proliferation of breast cancer cells, however the detailed mechanism renmins unknown. The aim of this study was to explore the effect of miR-27b on proliferation of breast cancer MCF-7 cells. Methods miR-27b mimic was transfected into MCF-7 cells by lipofectamine 2000, then the expression of miR-27b was detected by Real-time PCR. The expression of PPARγ and NHE1 was detected by Western Blot and cell proliferation was detected by CCK-8 assay. Results The miR-27b level was increased significantly in the MCF-7 cells transfected with miR-27b mimic with significant downregulation of PPARγ and significant upregulation of NHE1 (P 〈 0.05, respectively). The result of CCK8 assay showed that miR-27b mimic can efficiently promot MCF-7cell proliferation (P 〈 0.05). Conclusion miR-27b could inhibit the MCF-7cell proliferation via repressing PPARγ expression and promoting NHE1 expression.
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