MOLECULAR MECHANISM OF MIR-7 INHIBITING EMT AND INVASION AND METASTASIS OF GASTRIC CANCER CELLS BY REGULATING IGF1R EXPRESSION

Objective: Investigate how miR-7 inhibits epithelial mesenchymal transition (EMT) and the invasion and metastasis of gastric cancer cells by regulating the expression of IGF1R. Methods: Gastric adenocarcinoma cell line gc9811-p was selected to construct four cell models: overexpression of miR-7, overexpression of control, inhibition of miR-7 and inhibition of control. The migration and invasion abilities of each group were observed via Transwell cell migration tests. The expressions of E-cadherin, I3-catenin, vimentin and IGF1R were detected. The expression of snail, slug, ZEB1 and ZEB2 genes were detected via real-time quantitative PCR. Results: The migration ability of gastric cancer cells in the miR-7 overexpression group was significantly lower than that measured in the overexpression control group, and the migration ability of gastric cancer cells in the inhibition group was significantly higher than that measured in the control group (P<0.05). The invasion ability of gastric cancer cells in the miR-7 overexpression group was significantly lower than that measured in the overexpression control group, and the invasion ability of gastric cancer cells in the inhibition of miR-7 group was significantly higher than that measured in the control group (P<0.05). The contact between gc9811-p cells in the miR-7 overexpression group was closer than that measured in the overexpression control group. The expression levels of E-cadherin and I3-catenin in the overexpression group were significantly higher than those measured in the overexpression control group, and the vimentin expression level was significantly lower than that measured in the overexpression control group. The expression levels of E-cadherin and I3-catenin in the inhibition group were significantly lower than those in the overexpression control group, and the vimentin expression level was significantly higher than that measured in the overexpression control group (P<0.05). A Western blot analysis showed that miR-7 could inhibit the overexpression of wild-type IGF1R in gc9811 cells, but could not inhibit the expression of mutant IGF1R. The expression of the snail gene in the miR-7 overexpression group was significantly lower than that measured in the overexpression control group (P<0.05). Conclusion: The overexpression of miR-7 can inhibit the migration and invasion of gastric cancer cells and inhibit the EMT process of gastric cancer cells by regulating EMT related markers such as E-cadherin, I3-catenin and vimentin. The mechanism may be related to the regulation of IGF1R expression by miR-7.