南方医科大学学报
南方醫科大學學報
남방의과대학학보
JOURNAL OF SOUTHERN MEDICAL UNIVERSITY
2014年
2期
218-222
,共5页
谢强%黄作平%闫雍容%李锋%钟雪云
謝彊%黃作平%閆雍容%李鋒%鐘雪雲
사강%황작평%염옹용%리봉%종설운
胶质瘤%miR-221%PETN%Akt%上皮间质转化%多药耐药
膠質瘤%miR-221%PETN%Akt%上皮間質轉化%多藥耐藥
효질류%miR-221%PETN%Akt%상피간질전화%다약내약
glioma%miR-221%PETN%Akt%epithelial-mesenchymal transition%multi-drug resistance
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、E-cadherin、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。
目的:探討miR-221在耐藥膠質瘤細胞中與上皮間質轉化的相關性。方法熒光定量PCR和蛋白免疫印跡分析方法比較人膠質瘤細胞株Z1(原髮性耐藥細胞株)、Z2(藥物敏感細胞株)和Z2-BCNU(耐藥細胞株)中miR-221、PTEN、p-Akt、E-cadherin、vimentin、MRP1錶達的差異。結果 PTEN在Z2細胞中蛋白錶達含量明顯高于miR-221、vimentin高錶達的Z1和Z2-BCNU細胞,在E-cadherin高錶達的Z2細胞中vimentin、p-Akt和MRP1含量明顯減低。結論 MiR-221通過下調PTEN激活PI3-K/Akt信號從而調控上皮間質轉化相關基因的錶達。
목적:탐토miR-221재내약효질류세포중여상피간질전화적상관성。방법형광정량PCR화단백면역인적분석방법비교인효질류세포주Z1(원발성내약세포주)、Z2(약물민감세포주)화Z2-BCNU(내약세포주)중miR-221、PTEN、p-Akt、E-cadherin、vimentin、MRP1표체적차이。결과 PTEN재Z2세포중단백표체함량명현고우miR-221、vimentin고표체적Z1화Z2-BCNU세포,재E-cadherin고표체적Z2세포중vimentin、p-Akt화MRP1함량명현감저。결론 MiR-221통과하조PTEN격활PI3-K/Akt신호종이조공상피간질전화상관기인적표체。
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.