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

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.