MicroRNA-215 suppresses the proliferation, migration and invasion of non-small cell lung carcinoma cells through the downregulation of matrix metalloproteinase-16 expression

Abstract

The present study investigated the expression of microRNA (miR)‑215 in non‑small cell lung carcinoma (NSCLC) at tissue and cellular levels, as well as its biological functions and mechanism of action. A total of 56 patients with NSCLC were included in the present study. NSCLC tissues and tumor‑adjacent normal tissues were resected and collected. Reverse transcription‑quantitative polymerase chain reaction was used to measure the expression of miR‑215. Following transfection with miR‑215 mimics, A549 cell proliferation, migration and invasion were determined using a Cell Counting Kit‑8 and Transwell assay. Western blotting was employed to measure the expression of matrix metalloproteinase (MMP)‑16 protein. A dual‑luciferase reporter assay was conducted to determine the existence of a direct interaction between miR‑215 and the MMP‑16 gene. Reduced expression of miR‑215 in NSCLC was closely associated with lymphatic metastasis and TNM staging. Overexpression of miR‑215 inhibited the proliferation of A549 cells in vitro. Upregulated expression of miR‑215 inhibited the migration and invasion of A549 cells in vitro. miR‑215 exerted its biological functions possibly by regulating the expression of MMP‑16. Elevated expression of MMP‑16 promoted the proliferation, migration and invasion of A549 cells. miR‑215 regulated the proliferation, migration and invasion of A549 cells by binding with the seed 3'‑untranslated region of MMP‑16 mRNA. The present study demonstrates that reduced expression of miR‑215 in NSCLC is negatively associated with lymphatic metastasis and TNM staging. In addition, miR‑215 acts as a tumor suppressor gene by inhibiting the proliferation, migration and invasion of NSCLC cells via the downregulation of MMP‑16 expression.