miR-205对黑色素瘤A375细胞增殖、黏附和迁移的影响及机制探讨  

miRNA-205 suppresses melanoma cell line A375 proliferation,adhesion and migration via PTEN/AKT pathway

作　　者：孙慧娟 胡纯婷[2] 吴共发[3] 

机构地区：[1]中山市阜沙医院,广东中山510632 [2]南方医科大学基础医学院 [3]中山大学附属博济医院

出　　处：《山东医药》2012年第44期23-25,28,I0001,共5页Shandong Medical Journal

摘　　要：目的探讨miR-205对人皮肤恶性黑色素瘤细胞系A375增殖、黏附和迁移的影响及其可能机制。方法将miR-205 mimics用阳离子脂质体LipofectamineTM2000转染A375细胞,CCK-8法测细胞增殖变化;细胞黏附实验和划痕实验检测细胞黏附和迁移能力变化。Western blot检测PTEN、总AKT和磷酸化AKT蛋白表达变化。结果上调miR-205表达后实验组的细胞增殖、黏附和迁移能力均比空白对照组和阴性对照组减低(P均<0.05);Western blot结果显示上调miR-205表达能增加PTEN蛋白表达,减低磷酸化AKT蛋白水平,但对非AKT蛋白表达无影响。结论 miR-205可能通过调控PTEN/AKT通路抑制黑色素瘤细胞的增殖、黏附和迁移能力。Objective To investigate the effects of miR-205 on proliferation, adhesion and migration in human skin malignant melanoma cell line A375 and further elucidate its mechanisms. Methods miR-205 mimics was transfected A375 by lipofectamine package. Cell proliferation was studied by Cell Counting Kit-8 （CCK-8） assay. The wound migra- tion assay and adhesion assay were utilized to analyze the migration and adhesion of A375 cells in vitro after miR-205 over- expression. The expressions of proteins were investigated by Western blot. Results miR-205 significantly inhibited cell proliferation, adhesion and migration. PTEN protein was markedly increased and the phosphorylation of AKT was markedly reduced by miR-205 mimics treatment, respectively. But miR-205 had no effect on unphosphorylated AKT. Conclusion miR-205 exhibits inhibitory effects on proliferation, adhesion and migration in human skin malignant melanoma cell line, and its action mechanisms may involve in PTEN/AKT pathway.

关 键 词：黑色素瘤 细胞系 微小RNA 

分 类 号：R739.5[医药卫生—肿瘤]