医药前沿
醫藥前沿
의약전연
YIAYAO QIANYAN
2014年
20期
130-132
,共3页
郑娜芬%林俊汕%郭佳琳%叶梓莹
鄭娜芬%林俊汕%郭佳琳%葉梓瑩
정나분%림준산%곽가림%협재형
葡萄膜黑素瘤%miR-137%增殖%迁移
葡萄膜黑素瘤%miR-137%增殖%遷移
포도막흑소류%miR-137%증식%천이
uveal melanoma%miR-137%proliferation%migration
目的:探讨人眼葡萄膜黑素瘤细胞系M23转染m i R-137后对细胞增殖和迁移能力的影响及其分子机制的初探。方法:采用阳离子脂质体LipofectamineTM2000将miR-137mimics转染M23细胞,应用CCK-8法检测转染后细胞增殖变化,划痕实验检测细胞迁移能力变化。Westernblot检测PTEN、总AKT和磷酸化AKT蛋白表达。结果:转染miR-137后,实验组的细胞增殖较对照组明显减低(t=-18.754,P=0.000;);在36h和72h时间点,实验组细胞的划痕愈合程度均明显低于对照;实验组的PTEN蛋白表达增加,p-AKT蛋白减低,AKT蛋白表达无明显变化。结论:miR-137通过上调PTEN蛋白表达和减低AKT磷酸化活性从而抑制人眼葡萄膜黑素瘤细胞的增殖和迁移能力。
目的:探討人眼葡萄膜黑素瘤細胞繫M23轉染m i R-137後對細胞增殖和遷移能力的影響及其分子機製的初探。方法:採用暘離子脂質體LipofectamineTM2000將miR-137mimics轉染M23細胞,應用CCK-8法檢測轉染後細胞增殖變化,劃痕實驗檢測細胞遷移能力變化。Westernblot檢測PTEN、總AKT和燐痠化AKT蛋白錶達。結果:轉染miR-137後,實驗組的細胞增殖較對照組明顯減低(t=-18.754,P=0.000;);在36h和72h時間點,實驗組細胞的劃痕愈閤程度均明顯低于對照;實驗組的PTEN蛋白錶達增加,p-AKT蛋白減低,AKT蛋白錶達無明顯變化。結論:miR-137通過上調PTEN蛋白錶達和減低AKT燐痠化活性從而抑製人眼葡萄膜黑素瘤細胞的增殖和遷移能力。
목적:탐토인안포도막흑소류세포계M23전염m i R-137후대세포증식화천이능력적영향급기분자궤제적초탐。방법:채용양리자지질체LipofectamineTM2000장miR-137mimics전염M23세포,응용CCK-8법검측전염후세포증식변화,화흔실험검측세포천이능력변화。Westernblot검측PTEN、총AKT화린산화AKT단백표체。결과:전염miR-137후,실험조적세포증식교대조조명현감저(t=-18.754,P=0.000;);재36h화72h시간점,실험조세포적화흔유합정도균명현저우대조;실험조적PTEN단백표체증가,p-AKT단백감저,AKT단백표체무명현변화。결론:miR-137통과상조PTEN단백표체화감저AKT린산화활성종이억제인안포도막흑소류세포적증식화천이능력。
Objective To study the effects of miR-137 on proliferation and migration in human uveal malignant melanoma celllines M23 and investigate its action mechanisms.Methods miR-137 mimics were transfected M23 by LipofectamineTM 2000. The change of cellproliferation and migration of M23 cells were studied by cellCounting Kit-8 (CCK-8) assay and wound migration assay, respectively. PTEN, p-AKT and AKT proteins expression were investigated by western blot. Results miR-137 significantly inhibited cellproliferation and migration. PTEN protein was markedly increased and the phosphorylation of AKT was markedly reduced by miR-137 mimics treatment, respectively, but miR-137 was no effect on unphosphorylated AKT. Conclusion miR-137 exhibits inhibitory effects on proliferation and migration in human uveal melanoma cellthrough up-regulated PTEN protein expression and inhibit the phosphorylation of AKT.