miR-147a suppresses the metastasis of non-small-cell lung cancer by targeting CCL5

• Published in: Journal of international medical research Vol. 48; no. 4; p. 300060519883098
• Main Authors: Lu, Yan, Luan, Xiao Rong
• Format: Journal Article
• Language: English
• Published: London, England SAGE Publications 01.04.2020; Sage Publications Ltd
• Subjects: Animals; Carcinoma, Non-Small-Cell Lung - genetics; Cell Line, Tumor; Cell Movement; Cell Proliferation; Chemokine CCL5; Humans; Lung cancer; Lung Neoplasms - genetics; Metastasis; Mice; MicroRNAs; MicroRNAs - genetics; Neoplasm Transplantation; Pre-Clinical Research Report; NSCLC; invasion; metastasis; CCL5; miR-147a; migration; C-C motif chemokine ligand 5; non-small-cell lung cancer
• ISSN: 0300-0605; 1473-2300
• DOI: 10.1177/0300060519883098

Objective MicroRNA (miR)-147a acts as an inhibitory miRNA in many cancers. However, its potential roles in non-small-cell lung cancer (NSCLC) remain unclear. Methods Levels of miR-147a and C-C motif chemokine ligand 5 (CCL5) were measured using a quantitative real-time PCR assay. Cell growth, migration, and invasion of NSCLC cells were assessed by colony formation, wound healing, and Transwell invasion assays, respectively. The role of miR-147a in the growth and metastatic ability of NSCLC in vivo was detected using a xenograft model and experimental lung metastasis model. Results miR-147a was downregulated in NSCLC cell lines as well as in tissues. Gain-of-function and loss-of-function analyses demonstrated that upregulation of miR-147a decreased the aggressiveness of NSCLC cells in vitro. In addition, CCL5 was identified as a target of miR-147a. We also demonstrated the effect of miR-147a in the progression of NSCLC cells via targeting CCL5. Finally, the in vivo mouse xenograft model showed that miR-147a inhibited progression of NSCLC cells. Conclusions Overall, expression of miR-147a was downregulated in NSCLC. Importantly, upregulation of miR-147a suppressed the growth and metastasis of NSCLC cells in vivo by targeting CCL5.