Onco-miR-130 promotes cell proliferation and migration by targeting TGFβR2 in gastric cancer
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Jingjing Duan1,*, Haiyang Zhang1,*, Yanjun Qu1,*, Ting Deng1, Dingzhi Huang1, Rui Liu1, Le Zhang1, Ming Bai1, Likun Zhou1, Guoguang Ying1, Yi Ba1
1Department of Gastrointestinal Oncology, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Tianjin Key Laboratory of Cancer Prevention and Therapy, Tianjin, 300060, China
*These authors have contributed equally to this work
Yi Ba, email: firstname.lastname@example.org
Guoguang Ying, email: email@example.com
Keywords: TGFβR2, miR-130, gastric cancer, proliferation, migration
Received: December 13, 2015 Accepted: May 20, 2016 Published: June 10, 2016
MicroRNAs (miRNAs) have been proved to play crucial roles in tumorigenesis. TGFβ signal pathway abnormality is found in various cancers and correlates with tumor proliferation and metastasis. However, the mechanisms underlying the dys-regulation of TGFβR2 expression in GC have not been investigated yet. In this study, we found that the TGFβR2 protein was clearly repressed in tumor tissues, while miR-130 expression level was dramatically increased in GC tissues. Firefly luciferase activity assay revealed that miR-130 could directly bind to 3′UTR of TGFβR2 mRNA. Meanwhile, miR-130 mimics lead to the decreased TGFβR2 protein levels, while miR-130 inhibitors enhanced TGFβR2 expression in SGC7901 cells. Subsequent functional experiments showed that overexpressed miR-130 could promote proliferation and migration of SGC7901 cells. And siRNA-mediated TGFβR2 down-regulation could simulate the effects of miR-130 mimics on phenotypes of SGC7901 cells. Furthermore, there existed intense relationship between the expression level of miR-130 and epithelial-mesenchymal markers. Our results demonstrated that miR-130 was an oncogene by directly targeting TGFβR2 in GC.
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