miR-769-5p suppressed cell proliferation, migration and invasion by targeting TGFBR1 in non-small cell lung carcinoma
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Zhao Yang1,*, Jin He2,*, Peng Gao1, Yi Niu1, Jie Zhang3, Lei Wang3, Meiyue Liu1, Xiaomei Wei1, Chunling Liu3, Chao Zhang1, Wei Wang1, Jiayi Du3, Hongmin Li3, Wanning Hu1 and Guogui Sun1
1Department of Radiation Oncology, North China University of Science and Technology Affiliated People's Hospital, Tangshan, China
2Department of Hepatobiliary Tumor, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Cencer, Tianjin, China
3Department of Pathology, North China University of Science and Technology Affiliated People's Hospital, Tangshan, China
*These authors share co-first authorship
Wanning Hu, email: firstname.lastname@example.org
Guogui Sun, email: email@example.com
Keywords: lung cancer; microRNAs; invasion and metastasis; gene therapy
Received: July 27, 2017 Accepted: November 14, 2017 Published: December 08, 2017
MicroRNAs (miRNAs) are key regulators of multiple cancers, including non-small cell lung carcinoma (NSCLC). The aim of this study was to determine the expression pattern of miR-769-5p in NSCLC and to investigate its biological role during tumorigenesis. We showed that miR-769-5p was significantly downregulated and predicted poor prognosis in NSCLC compared with corresponding normal tissues. We then investigated its function and found that miR-769-5p significantly inhibited cell proliferation, migration and invasion in vitro and reduced tumor growth and metastasis in vivo. Furthermore, we explored the molecular mechanisms by which miR-769-5p contributes to NSCLC suppression and identified TGFBR1 as a direct target gene of miR-769-5p. Finally, we showed that TGFBR1 had opposite effects to those of miR-769-5p on lung cancer cells, suggesting that miR-769-5p might inhibit lung tumorigenesis by silencing TGFBR1. Taken together, our results demonstrated that miR-769-5p plays a pivotal role in NSCLC by inhibiting cell proliferation, migration and invasion by targeting TGFBR1.
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