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作 者:李燕[1] 刘龙山[2] 郝泽蕊[1] 吕培瑾[1] 王淑云[1] 杨福堂[1]
机构地区:[1]山东省聊城市第二人民医院呼吸内科,山东聊城252600 [2]中山大学附属第一医院外科实验室,广东广州510000
出 处:《武汉大学学报(医学版)》2014年第2期198-201,共4页Medical Journal of Wuhan University
摘 要:目的:探讨microRNA-429(miR-429)对人肺癌A549细胞增殖和凋亡的影响。方法:定量逆转录聚合酶链反应(qPCR)技术检测A549细胞瞬时转染miR-429mimic或inhibitor后miR-429的表达;通过MTT法和流式细胞术检测转染后细胞增殖能力和凋亡变化。结果:瞬时转染miR-429mimic 24h后,qPCR结果显示miR-429表达显著升高(9.3±0.3比1.0±0.1,P<0.05),而转染miR-429inhibitor可以显著降低miR-429表达(0.3±0.0比1.0±0.1,P<0.05);与对照组相比,过表达miR-429抑制肿瘤细胞增殖(2.8±0.2比5.0±0.3,P<0.05)并诱导凋亡(18.9±1.2比12.3±1.0,P<0.05),而下调miR-429表达促进肿瘤细胞增殖(6.3±0.4比5.0±0.3,P<0.05)并抑制凋亡(7.1±0.6比12.3±1.0,P<0.05)。结论:miR-429在肺癌中可能作为肿瘤抑制因子发挥功能。Objective: To investigate the effect oI microRNA-429 (mlN-4Zg) on the proliferation and ap optosis of lung cancer cells. Methods: We detected expression of miR-429 after miR-429 mimic and its inhibitor were transiently transfected into human lung cancer cell line A549. The cell proliferation and apoptosis after transfection were analyzed by MTT and flow cytometry. Results: 24 h after miR-429 mimic transfection, the expression of miR-429 was significantly up-regulated (9.3±0.30 vs 1.0±0.08, P〈0.05). However, miR-429 inhibitor transfection led to downregulation of miR-429(0.3±0.05 vs 1.0±0.08, P〈0.05). Compared with control transfection, miR-429 overexpression inhibited tumor cell proliferation (2.8±0.21 vs 5.04±0.27, P〈0.05) and induced cell apoptosis significantly (18.9±1.2 vs 12.3±1.0, P〈0.05). On the contrary, downregulation of miR-429 promoted tumor cell proliferation (6.3 ± 0.35 vs 5.0 ±0.27, P〈 0.05) and inhibited cell apoptosis significantly (7.1±0.6 vs 12.3±1.0, P〈0.05). Conclusion: MiR-429 may serve as a tumor suppressor and may be a potential therapeutic target in lung cancer.
关 键 词:microRNA-429 肺癌 增殖 凋亡
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