MicroRNA-16 inhibits the proliferation, migration and invasion of non-small cell lung carcinoma cells by down-regulating matrix metalloproteinase-19 expression

G. Tian, S.-W. Wang, M. Song, Y.-F. Hu, X.-N. Cao, J.-W. Ge

Department of Respiratory Medicine, Affiliated Hospital of Jining Medical University, Jining, China. jiyijiwen5@163.com

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• Oncology

OBJECTIVE: This study aims to investigate the expression of microRNA (miR)-16 in non-small cell lung carcinoma (NSCLC) and to identify its potential mechanism.
PATIENTS AND METHODS: A total of 45 NSCLC patients were included in the present work. NSCLC tissues and adjacent normal tissues were resected and collected. The Reverse Transcription-quantitative Polymerase Chain Reaction was used to determine miR-16 expression. Regulatory effects of miR-16 on proliferation, migration and invasion, and cell cycle of A549 cells were determined by Cell-Counting Kit 8 assay, transwell assay, and flow cytometry, respectively. Western blotting was performed to measure the protein expression of matrix metalloproteinase (MMP)-19 in cells overexpressing miR-16. Dual-luciferase reporter gene assay was conducted to identify the interaction between miR-16 and MMP-19.
RESULTS: MiR-16 expression in NSCLC significantly decreased compared with that in healthy tissue (p<0.05). The expression level of miR-16 was negatively correlated to the clinical staging of NSCLC. In addition, the expression of miR-16 in NSCLC patients with lymph node metastasis was significantly lower than that in patients without lymph node metastasis (p<0.05). In vitro studies demonstrated that miR-16 inhibited the proliferation, migration, and invasion of A549 cells. Western blotting analyses indicated that overexpression of miR-16 down-regulated the expression of MMP-19. Additionally, the dual-luciferase reporter gene assay determined that miR-16 directly regulated the expression of MMP-16.
CONCLUSIONS: The present study demonstrates that miR-16 acts as a tumor-suppressor gene by inhibiting the proliferation, migration, and invasion of NSCLC cells via downregulating MMP-19 expression.

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