miR‑497 suppresses malignant phenotype in non‑small cell lung cancer via targeting KDR

The aim of the present study was to evaluate the expression of microRNA‑497 (miR‑497) in non‑small cell lung cancer (NSCLC) tissues and cell lines, and to investigate possible mechanisms associated with its regulatory role on cell behaviors. The expression level of miR‑497 was evaluated in 15 cases of NSCLC tissues and 8 adjacent normal tissues, and in 8 NSCLC cell lines, including H1975, A549, H358, H1650, H460, Calu‑1, H1299 and H292, by reverse transcription‑quantitative polymerase chain reaction. Effects of miR‑497 overexpression on cell proliferation, invasion, apoptosis and radiosensitivity were examined with a Cell Counting Kit‑8 assay, Matrigel assay, flow cytometry and a clone formation assay in vitro, respectively, and in an in vivo ectopic tumor nude mice model. A dual luciferase reporter assay was employed for interaction between miR‑497 and its target gene kinase insert domain receptor (KDR). A significantly decreased level of miR‑497 was determined in NSCLC tissues, compared with adjacent normal tissues, and Calu‑1 and H1975 exhibited the lowest miR‑497 expression among the 8 NSCLC cell lines. miR‑497 overexpression could inhibit cell proliferation and invasion, promote cancer cell apoptosis and decrease cell clone formation following radiation treatment in vitro, and decrease tumor growth in vivo. Furthermore, a dual luciferase reporter assay revealed that KDR as the target gene for miR‑497. It was demonstrated that miR‑497 was downregulated in NSCLC specimens. Additionally, miR‑497 directly targeted and downregulated KDR expression, and inhibited malignant behaviors of NSCLC cells. These data indicated that miR‑497 could serve as a tumor suppressor gene involved in NSCLC pathogenesis.