miR-143 and miR-145 inhibit gastric cancer cell migration and metastasis by suppressing MYO6

Chao Lei(National Clinical Research Center for Digestive Diseases), Feng Du(National Clinical Research Center for Digestive Diseases), Lina Sun(National Clinical Research Center for Digestive Diseases), Ting Li(National Clinical Research Center for Digestive Diseases), Tingyu Li(National Clinical Research Center for Digestive Diseases), Yali Min(National Clinical Research Center for Digestive Diseases), Aiying Nie(National Clinical Research Center for Digestive Diseases), Xin Wang(National Clinical Research Center for Digestive Diseases), Lei Geng(National Clinical Research Center for Digestive Diseases), Yuanyuan Lu(National Clinical Research Center for Digestive Diseases), Xiaodi Zhao(National Clinical Research Center for Digestive Diseases), Yongquan Shi(National Clinical Research Center for Digestive Diseases), Daiming Fan(National Clinical Research Center for Digestive Diseases)
Cell Death and Disease
October 12, 2017
Cited by 173Open Access
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Abstract

Metastasis is a major clinical obstacle responsible for the high mortality and poor prognosis of gastric cancer (GC). MicroRNAs (miRNAs) are critical mediators of metastasis that act by modulating their target genes. In this study, we found that miR-143 and miR-145 act via a common target gene, MYO6, to regulate the epithelial-mesenchymal transition (EMT) and inhibit metastasis. We determined that miR-143 and miR-145 were downregulated in GC, and the ectopic expression of miR-143 and/or miR-145 inhibited GC cell migration and metastasis. Furthermore, MYO6 was identified as a direct common target of miR-143 and miR-145 and was elevated in GC. Silencing of MYO6 resulted in a metastasis-suppressive activity similar to that of miR-143 and miR-145, while restoring MYO6 attenuated the anti-metastatic or anti-EMT effects caused by miR-143 and miR-145. Clinically, an inverse correlation was observed between miR-143/145 levels and MYO6 levels in GC tissues, and either miR-143/145 downregulation or MYO6 upregulation was associated with more malignant phenotypes in patients with GC. In conclusion, miR-143 and miR-145 suppress GC cell migration and metastasis by inhibiting MYO6 expression and the EMT, which provides a novel mechanism and promising therapeutic target for the treatment of GC metastasis.


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