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miR-769-5p suppressed cell proliferation, migration and invasion by targeting TGFBR1 in non-small cell lung carcinoma

Zhao Yang, Jin He, Peng Gao, Yi Niu, Jie Zhang, Lei Wang, Meiyue Liu, Xiaomei Wei, Chunling Liu, Chao Zhang, Wei Wang, Jiayi Du, Hongmin Li, Wanning Hu _ and Guogui Sun

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Oncotarget. 2017; 8:113558-113570. https://doi.org/10.18632/oncotarget.23060

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Abstract

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

Correspondence to:

Wanning Hu, email: [email protected]

Guogui Sun, email: [email protected]

Keywords: lung cancer; microRNAs; invasion and metastasis; gene therapy

Received: July 27, 2017     Accepted: November 14, 2017     Published: December 08, 2017

ABSTRACT

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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