microRNA-100对人胰腺癌细胞增殖及皮下成瘤能力的影响

MicroRNA-100 Inhibiting Pancreatic Cancer Cell Proliferation and Tumorigenicity

目的:研究microRNA-100(miR-100)对人胰腺癌细胞MIA Pa Ca-2和CFPAC-1增殖及皮下成瘤能力的影响。方法:用miR-100慢病毒过表达载体感染MIA Pa Ca-2和CFPAC-1细胞,构建高表达miR-100细胞株;用平板克隆、CCK-8方法检测miR-100对人胰腺癌细胞体外增殖能力,裸鼠皮下成瘤实验检测miR-100对人胰腺癌细胞成瘤能力。结果:慢病毒感染后,miR-100表达在MIA Pa Ca-2细胞中提高(941±171)倍,在CFPAC-1细胞中提高(154±23)倍,差异有统计学意义(P<0.05);平板克隆形成实验提示MIA Pa Ca-2和CFPAC-1细胞实验组平板克隆数少于对照组病毒,差异有统计学意义(P<0.05);CCK-8细胞增殖实验提示MIA Pa Ca-2和CFPAC-1细胞实验组增殖能力弱于对照组,差异有统计学意义(P<0.05);裸鼠皮下成瘤实验显示,miR-100抑制了肿瘤裸鼠皮下成瘤。结论:miR-100能从体内外抑制人胰腺癌细胞增殖及皮下成瘤能力。

Objective：To investigate the effects of miR-100 on proliferation and tumorigenicity of MIA PaCa-2 and CFPAC-1 cells. Methods：Using miR-100 lentivirus overexpression vector to infect MIA PaCa-2 and CFPAC-1 cells to establish miR-100 cell strain. Pancreatic cancer cell proliferation was analyzed using CCK-8 and colony formation assay. BALB/c Nude mice subcutaneous tumor exper-iment was adopted to test the effect of micorRNA-100 on HPCC. Results：The expression of miR-100 after infected by miR-100 lentivirus was（941 ± 171）folds in MIA PaCa-2 cells,and（154 ± 23）folds in CFPAC-1 cells,the differences were statistically significant（P ﹤0. 05）. Colony formation assay prompted the number of clones of MIA PaCa-2 and CFPAC-1 cells in experimental group were less than the control group,the difference was statistically significant（P﹤0. 05）;CCK-8 cell proliferation ex-periments suggested that MIA PaCa-2 and CFPAC-1 cell proliferation in the experimental group was weaker than that of control group,difference was statistically significant（P﹤0. 05）. Nude mice sub-cutaneous tumor experiment suggested that miR-100 inhibited tumor growth. Conclusions：miR-100 can inhibit human pancreatic cancer cell proliferation and tumorigenicity.