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Chinese Journal of Pathophysiology ; (12): 1191-1195, 2017.
Article in Chinese | WPRIM | ID: wpr-616499

ABSTRACT

AIM: To investigate the inhibitory effect of microRNA-9 (miR-9) on epithelial-mesenchymal transition (EMT) in the gastric cancer SGC-7901 cells and its mechanism.METHODS: The gastric cancer cell line SGC-7901 was transfected with miR-9 mimics or negative control mimic (NCM), as miR-9 or NCM group, respectively.The SGC-7901 cells without transfection were used as control group.The expression level of miR-9 in each group was detected by RT-qPCR.The migration and invasion abilities of the SGC-7901 cells in the 3 groups were detected by Transwell assay.The protein expression of N-cadherin, E-cadherin, α-catenin and neuropilin-1 (NRP1) was determined by Western blot.Antagonistic effect of NRP1 over-expression on miR-9 inhibition of EMT was detected by Western blot.The relationship between miR-9 and NRP1 was analyzed by dual luciferase assay.RESULTS: The expression level of miR-9 in miR-9 group was significantly up-regulated, which was 538 times higher than that in control group (P<0.05).The number of migratory cells in miR-9 group was significantly lower than that in control group (P<0.05).Compared with control group, the protein expression of N-cadherin and NRP1 in miR-9 group was significantly decreased, while the protein expression of E-cadherin and α-catenin protein was significantly increased.Over-expression of NRP1 resulted in the increase in the protein expression of N-cadherin in the gastric cancer cells of miR-9 group, and the decrease in the protein expression of E-cadherin and α-catenin significantly.The result of dual luciferase assay showed that NRP1 was a downstream target gene of miR-9 (P<0.05).CONCLUSION: miR-9 may inhibit the expression of EMT-related proteins through the downstream target gene NRP1, thus inhibiting the EMT of gastric cancer SGC-7901 cells.

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