Antitumor effects of hsa‑miR661‑3p on non‑small cell lung cancer in vivo and in vitro.

Abstract

Lung cancer is the most common and lethal cancer worldwide, especially in developing countries. Non‑small cell lung cancer (NSCLC) accounts for 85% of all cases of lung cancer. In aprevious study, the protein expression of ubiquitin conjugating enzyme E2 C (UBE2C/UbcH10) in NSCLC tissues and cells was found to be significantly higher than that in adjacent tissues and normal lung epithelial cells. Further study revealed that the aberrant expression of UbcH10 in NSCLC tumors or cancer cells was caused by inactivation of the post‑transcriptional regulation mechanism, and thus microRNAs (miRNAs) may play an important. In the present study, it was demonstrated that the expression of microRNA, hsa‑miR661‑3p, was downregulated and UbcH10 was upregulated in 12 pairs of NSCLC tumors and three NSCLC cell lines. A reporter gene assay revealed that overexpression of hsa‑miR661‑3p effectively reduced the activity of luciferase expressed by a vector bearing the 3' untranslated region of UbcH10 mRNA. Ectopic hsa‑miR661‑3p overexpression mediated by lentiviral infection decreased the expression of UbcH10. Infection of Lv‑miR661‑3p inhibited cell growth and invasion in A549 and SK‑MES‑1 cells. Mechanistically, hsa‑miR661‑3p induced cell cycle G2 arrest through regulation of spindle assembly checkpoint (SAC) function. On the basis of the proposed mechanisms, the objective of the study was to inhibit the proliferation of A549 and SK‑MES‑1 by expressing hsa‑miR661‑3p in vivo and in vitro. Collectively, our results indicated that downregulation of hsa‑miR661‑3p was involved in NSCLC and restoration of hsa‑miR661‑3p impaired the growth of NSCLC cell lines A549 and SK‑MES‑1, suggesting that hsa‑miR661‑3p may be a potential target molecule for the therapy of NSCLC.