MicroRNA-630 Suppresses Epithelial-to-Mesenchymal Transition by Regulating FoxM1 in Gastric Cancer Cells

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Jing Feng¹, Xiaojuan Wang², Weihua Zhu³, Si Chen³, and Changwei Feng^1*

¹The Second Affiliated Hospital of Zhengzhou University, Department of Gastroenterology, 450014 Zhengzhou, Henan Province, China; E-mail: fengchangwei373@126.com

²The First Affiliated Hospital of Zhengzhou University, Department of Oncology, 450052 Zhengzhou, Henan Province, China

³Zhengzhou YIHE Hospital, Department of Respiratory Medicine, 450047 Zhengzhou, Henan Province, China

^* To whom correspondence should be addressed.

Received October 9, 2016; Revision received January 18, 2017

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In the present study, we investigated the functional role of microRNA (miR)-630 in epithelial-to-mesenchymal transition (EMT) of gastric cancer (GC) cells, as well as the regulatory mechanism. Cells of human GC cell line SGC 7901 were transfected with miR-630 mimic or miR-630 inhibitor. The transfection efficiency was confirmed by qRT-PCR. Cell migration and invasion were determined by Transwell assay. Protein expression of E-cadherin, vimentin, and Forkhead box protein M1 (FoxM1) was tested by Western blot. Moreover, the expression of FoxM1 was elevated or suppressed, and then the effects of miR-630 abnormal expression on EMT and properties of migration and invasion were examined again, as well as protein expression of Ras/phosphoinositide 3-kinase (PI3K)/AKT related factors. The results showed that (i) the EMT and properties of migration and invasion were statistically decreased by overexpression of miR-630 compared to the control group but markedly increased by suppression of miR-630. However, (ii) abnormal expression of FoxM1 reversed these effects in GC cells. Moreover, (iii) expression of GTP-Rac1, p-PI3K, and p-AKT was decreased by miR-630 overexpression but increased by FoxM1 overexpression. (iv) The decreased levels of GTP-Rac1, p-PI3K, and p-AKT induced by miR-630 overexpression were dramatically elevated by simultaneous overexpression of FoxM1. In conclusion, our results suggest that miR-630 might be a tumor suppressor in GC cells. MiR-630 suppresses EMT by regulating FoxM1 in GC cells, supposedly via inactivation of the Ras/PI3K/AKT pathway.

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KEY WORDS: microRNA-630, gastric cancer, epithelial-to-mesenchymal transition, Forkhead box protein M1, migration and invasion

DOI: 10.1134/S0006297917060074

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