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上调miR-181a对胃癌细胞AGS增殖和凋亡的影响
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上调miR-181a对胃癌细胞AGS增殖和凋亡的影响
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Journal Article
上调miR-181a对胃癌细胞AGS增殖和凋亡的影响
2016
Overview
目的探讨miR-181a对胃癌细胞增殖、周期及凋亡的影响及其作用机制。方法荧光实时定量PCR检测5种胃癌细胞及人胃黏膜细胞系GES-1中miR-181a的表达情况,以及胃癌细胞AGS瞬时转染miR-181amimic后miR-181a的表达情况;MTT法和流式细胞仪检测上调miR-181a表达对胃癌细胞AGS增殖、周期和凋亡等生物学行为的影响;Western blot检测上调miR-181a后细胞周期调控蛋白（CDC25A、cyclinA2、cyclinD1、p21）和凋亡相关蛋白（Bcl-2和Bax）的表达变化。结果与人胃黏膜细胞系GES-1比较,miR-181a在人胃癌细胞株SGC-7901和MKN28表达升高（P均〈0.01）,在MGC-803、BGC-823、AGS表达差异无统计学意义（P均〉0.05）;瞬时转染miR-181amimic后,胃癌细胞AGS中miR-181a的表达明显上调（P〈0.05）;转染miR-181amimics后AGS细胞增殖明显,G0/G1期细胞减少,S期细胞明显增多,细胞凋亡明显减弱（P均〈0.05）。Western blot结果显示,上调miR-181a后胃癌细胞AGS中CDC25A、cyclinA2和Bcl-2表达升高（P均〈0.05）,cyclinD1和p21表达差异没有统计学意义（P〉0.05）,Bax表达降低（P〈0.05）。结论上调miR-181a可以促进胃癌细胞AGS增殖,其作用机制可能与CDC25A、CyclinA2表达升高有关;上调miR-181a可抑制胃癌细胞凋亡,其作用机制可能与Bcl-2表达升高及Bax表达降低有关。
