过表达miR-107促进HT29细胞增殖和成瘤能力

Overexpression of miR-107 promotes the proliferation and tumorigenic ability of HT29 cells

目的探讨微小RNA107(miR-107)对结肠癌细胞增殖的影响。方法实时定量PCR检测miR-107在结肠癌组织及NCM460、HT29、HCT116、SW480、Colo205和Lo Vo结肠癌细胞系的水平;培养HT29结肠癌细胞,分别转染miR-107模拟物(miR-107 mimic)、miR-107抑制物(miR-107 inhibitor),过表达或抑制miR-107后,通过噻唑蓝(MTT)实验、平板克隆实验检测细胞的增殖能力,软琼脂克隆形成实验及裸鼠成瘤实验检测HT29细胞的成瘤能力,Wetern blot法检测miR-107对HT29细胞中细胞周期蛋白D1(cyclin D1)的蛋白水平。结果 miR-107在结肠癌组织及多种结肠癌细胞中高表达。过表达miR-107增加HT29细胞的增殖能力及成瘤能力并上调细胞cyclin D1蛋白水平,抑制miR-107表达则可降低HT29细胞的增殖能力及成瘤能力。结论 miR-107在结肠癌组织及细胞中高表达,过表达的miR-107通过上调cyclin D1水平促进结肠癌细胞增殖及成瘤的作用。

Objective To investigate the effect of miR-107 on the proliferation of colorectal cancer cells. Methods The expression of miR-107 was detected in colorectal cancer tissues and colorectal cancer cell lines by real-time quantitative PCR( qRT-PCR). miR-107 expression was up-regulated and down-regulated by the transfection of miR-107 mimic and miR-107 inhibitor in HT29 cells,respectively. The effect of miR-107 on the proliferation of HT29 cells was evaluated by MTT assay.The tumorigenic ability of HT29 cells was detected by soft-agar colony formation assay and nude mouse tumorigenic assay.The expression of cyclin D1 in HT29 cells was tested by Western blot analysis. Results The expression of miR-107 wassignificantly up-regulated in both colorectal cancer tissues and cells. Overexpression of miR-107 promoted the proliferationand tumorigenicity of HT29 cells,while the decrease of miR-107 expression inhibited the proliferation and tumorigenicity ofHT29 cells. Overexpression of miR-107 up-regulated the expression of cyclin D1 in HT29 cells. Conclusion Overexpressionof miR-107 in both colon cancer tissues and cells promotes the proliferation and tumor formation potential of HT29 cells viaup-regulating cyclin D1 expression.