观察二甲双胍在高葡萄糖环境下对人结肠癌细胞系SW480增殖和侵袭的影响，并探讨其可能的机制。

通过Western blot方法检测SW480细胞在高葡萄糖及不同浓度二甲双胍干预后E-cadherin和Vimentin的表达水平，并应用CCK-8法及Transwell侵袭实验检测细胞增殖及侵袭能力的变化。

高葡萄糖作用不同时间后均能促进结肠癌细胞增殖，二甲双胍能抑制结肠癌细胞的增殖，并呈时间——剂量依赖性。20 mmol/L浓度二甲双胍干预48 h后，Transwell侵袭实验结果显示细胞穿膜数为（40.18±2.22）%，明显低于高糖组和对照组（F=49.403，P<0.001）；Western blot结果显示E-cadherin表达明显增强，Vimentin表达明显减弱。

高葡萄糖环境能促进结肠癌细胞生长，二甲双胍能明显抑制有或无高葡萄糖环境下结肠癌的增殖和侵袭能力，其机制可能与调节上皮——间质转化（EMT）过程有关。

To investigate the effects of metformin on proliferation and invasion in human colon carcinoma cell SW480 in the high glucose environment and explore the possible underlying mechanisms.

Western blot was applied to assess the expressions of E-cadherin and Vimentin in SW480 cells treated with high glucose medium and different concentration metformin, respectively. Cell proliferation and invasion were detected by Cell Counting Kit-8 (CCK-8) assay and transwell invasion assay, respectively.

High glucose could promote proliferation of SW480 cells at different action time. After intervened by different concentration of metformin, metformin decreased the proliferation of SW480 in a dose-and time dependent manner. Comparing with the high glucose group and control group, after 48 h of metformin (20 mmol/L) intervention to SW480, transwell invasion assay indicated that the cells crossing the membrane were significantly decreased to (40.18±2.22)% (F=49.403, P<0.001). Western blot showed that the expressions of E-cadherin were obviously increased, while Vimentin were apparently decreased.

High glucose environment can promote the growth of colon carcinoma cells. Metformin causes a distinct reduction of cells proliferation and invasion in colon carcinoma cells with or without high glucose environment, its molecular mechanism may involve in metformin have a role in the regulation of epithelial-mesenchymal transition.