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作 者:谢强[1,2] 黄作平[2] 闫雍容[1] 李锋[2] 钟雪云[1]
机构地区:[1]暨南大学医学院病理系,广东广州510632 [2]武警广东总队医院,广东广州510507
出 处:《南方医科大学学报》2014年第2期218-222,共5页Journal of Southern Medical University
基 金:国家自然科学基金(81072059)~~
摘 要:目的探讨miR-221在耐药胶质瘤细胞中与上皮间质转化的相关性。方法荧光定量PCR和蛋白免疫印迹分析方法比较人胶质瘤细胞株Z1(原发性耐药细胞株)、Z2(药物敏感细胞株)和Z2-BCNU(耐药细胞株)中miR-221、PTEN、p-Akt、Ecadherin、vimentin、MRP1表达的差异。结果 PTEN在Z2细胞中蛋白表达含量明显高于miR-221、vimentin高表达的Z1和Z2-BCNU细胞,在E-cadherin高表达的Z2细胞中vimentin、p-Akt和MRP1含量明显减低。结论 MiR-221通过下调PTEN激活PI3-K/Akt信号从而调控上皮间质转化相关基因的表达。Objective To investigate the correlation between miR-221 and epithelial-mesenchymal transition (EMT) in drug-resistant glioma cells. Methods The expression levels of miR-221, PTEN, p-Akt, E-cadherin, vimentin, and MRP1 were quantitatively analyzed in Z1 cells (primary drug-resistant cells), Z2 cells (drug-sensitive cells) and Z2-BCNU cells (drug-resistant cells) using fluorescent real-time PCR and Western blotting. Results The expression levels of PTEN were significantly increased in Z2 cells compared with Z1 and Z2-BCNU cells which overexpressed miR-221 and vimentin. The expression levels of vimentin, p-Akt and MRP1 were significantly decreased in Z2 cells overexpressing E-cadherin. Conclusion MiR-221 regulates the expression of EMT-related genes through down-regulation of PTEN and activation of PI3-K/Akt signaling.
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