miRNA-101-5p inhibits the growth and aggressiveness of NSCLC cells through targeting CXCL6
Authors Chen Q, Liu D, Hu Z, Luo C, Zheng SL
Received 16 August 2018
Accepted for publication 26 October 2018
Published 25 January 2019 Volume 2019:12 Pages 835—848
Checked for plagiarism Yes
Review by Single-blind
Peer reviewer comments 3
Editor who approved publication: Dr Leo Jen-Liang Su
Qi Chen,1,2 Dan Liu,3 Zhi Hu,4 Cheng Luo,1 Si Lin Zheng2
1State Key Laboratory of Quality Research in Chinese Medicine, Macau Institute for Applied Research in Medicine and Health, Macau University of Science and Technology, Macau, China; 2Department of Nursing, The Affiliated Hospital of Southwest Medical University, Sichuan, 646000, China; 3Department of Respiratory and Critical Care Medicine, Pulmonary and Critical Care Medicine, The Affiliated Hospital of Southwest Medical University, Sichuan, 646000, China; 4Department of Thoracic Surgery, The Affiliated Hospital of Southwest Medical University, Sichuan, 646000, China
Background: The purpose of this study is to explore the potential biological roles of miR-101-5p in the progression of non-small-cell lung carcinoma (NSCLC).
Methods: The levels of miR-101-5p and chemokine (C-X-C motif) ligand 6 (CXCL6) in NSCLC tissues and cells were detected using the quantitative real-time PCR (qRT-PCR) assay. Proliferation, colony formation, migration and invasion assays were conducted using miR-101-5p-transfected NSCLC cells in vitro. The expression of CXCL6 was measured using immunofluorescence assay. Xenograft model and lung metastasis model were constructed to further reveal the precise roles of miR-101-5p in the lung metastasis and growth of NSCLC cells in vivo.
Results: miR-101-5p was underregulated in NSCLC tissues when compared with that in the normal controls. The levels of miR-101-5p were lower in NSCLC cells (H1975, A549, HCC827 and H1650) than in non-tumorigenic human bronchial epithelial cells (BEAS-2B). Overregulation of miR-101-5p restrained the aggressiveness phenotypes of NSCLC cells in vitro. Furthermore, overregulation of miR-101-5p reduced the tumor growth and pulmonary metastasis of NSCLC cells in vivo. CXCL6 was the target gene of miR-101-5p in NSCLC. The mRNA levels of CXCL6 were negatively associated with the levels of miR-101-5p in NSCLC tissues. Finally, the rescue experiments suggested that the inhibitory role of miR-101-5p was mediated by regulating the expression of CXCL6 in NSCLC.
Conclusion: These findings indicated that overregulation of miR-101-5p restrained the progression of NSCLC cells by targeting CXCL6 and might function as a potential therapeutic target for NSCLC.
Keywords: lung cancer, miR-101-5p, CXCL6, metastasis
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