MiR‑495 suppresses cell proliferation by directly targeting HMGA2 in lung cancer.

Abstract

The present study aimed to investigate the expression of microRNA-495 (miR-495) in non-small cell lung cancer (NSCLC) tissues and cells, as well as its function on the proliferation of lung cancer cells. The expression of miR-495 in 122 pairs of NSCLC tissues and matched paracarcinoma tissues, as well as in human lung cancer cell lines (A549, H460, H1650, H520 and SK-MES-1) and the normal human pulmonary bronchial epithelial cell line 16HBE was determined using reverse transcription quantitative polymerase chain reaction (RT-qPCR). As predicted by bioinformatics analysis, high mobility group A2 (HMGA2) may be a potential target gene of miR-495. In addition, the regulatory function of miR-495 on its target gene HMGA2 was evaluated using a dual-luciferase reporter assay, RT-qPCR and western blotting. Furthermore, the effect of miR-495 on the proliferation of A549 lung cancer cells was investigated using a Cell Counting Kit-8 (CCK-8) assay. The results demonstrated that the expression of miR-495 in NSCLC tissues and cells was significantly downregulated compared with the control. In addition, downregulated expression of miR-495 was associated with tumor differentiation, lymph node metastasis and tumor, node and metastasis staging. Additionally, a dual-luciferase reporter assay revealed that miR-495 could directly associated with the 3′-untranslated region of HMGA2. Upregulated expression of miR-495 significantly downregulated the mRNA and protein expression levels of HMGA2 in A549 cells. Furthermore, the results of CCK-8 assay revealed that upregulated expression of miR-495 significantly suppressed the proliferation of A549 cells; HMGA2 overexpression reversed this inhibition. In summary, the findings of the present study demonstrated that miR-495 was downregulated in NSCLC tissues and cells. In addition, miR-495 suppressed the proliferation of lung cancer cells by directly targeting HMGA2.