Abstract
MicroRNAs (miRs) serve important roles in various human cancers, including lung adenocarcinoma. Exploring the function and regulatory mechanism of miRs underlying lung adenocarcinoma progression may contribute to identifying novel therapeutic targets and candidates. The present study aimed to examine miR-148a expression and investigate the molecular mechanisms of miR-148a in lung adenocarcinomas. The data from the current study indicated that miR-148a was significantly downregulated in lung adenocarcinoma tissues and cell lines, and low miR-148a expression was significantly associated with advanced Tumor, Node, Metastasis stages and lymph node metastasis, as well as the shorter survival time of patients. Increased miR-148a expression markedly decreased the cell proliferation, colony formation and cell cycle progression of H23 and H1975 cells. Transcription factor E2F3 (E2F3) was identified as a target of miR-148a in H23 and H1975 cells. The expression of E2F3 was negatively mediated by miR-148a in H23 and H1975 cells. In addition, E2F3 was significantly upregulated in lung adenocarcinoma tissues and cell lines, and the expression of miR-148a was inversely correlated with E2F3 expression in lung adenocarcinoma tissues. Additional experiments demonstrated that increased E2F3 expression counteracted the inhibitory effects on lung adenocarcinoma cells caused by miR-148a overexpression. In summary, the findings of the current study suggest that miR-148a may have suppressive effects on the proliferation of lung adenocarcinoma cells at least in part through directly targeting E2F3. Therefore, miR-148a may be used as a potential candidate for the treatment of lung adenocarcinoma.