Induction of microRNA‑let‑7a inhibits lung adenocarcinoma cell growth by regulating cyclin�D1

• DOI: 10.3892/or.2018.6593
• Publication Date: 2018-07-24T07:51:37Z
• Authors: Wei Zhao; Jin‑Xia Hu; Rui‑Min Hao; Qian Zhang; Jun‑Qi Guo; You‑Jie Li; Ning Xie; Lu‑Ying Liu; Ping‑Yu Wang; Can Zhang; Shu‑Yang Xie
• Keywords: Adult; Male; 0301 basic medicine; 0303 health sciences; Lung Neoplasms; Apoptosis; Articles; Cell Cycle Checkpoints; Adenocarcinoma; Middle Aged; Prognosis; 3. Good health; Gene Expression Regulation, Neoplastic; MicroRNAs; 03 medical and health sciences; Cell Movement; Case-Control Studies; Biomarkers, Tumor; Humans; Cyclin D1; Female; Neoplasm Invasiveness; Aged; Cell Proliferation; Follow-Up Studies

Lung cancer is the most common cause of cancer‑associated mortality. MicroRNAs (miRNAs), as oncogenes or tumor suppressor genes, serve crucial roles not only in tumorigenesis, but also in tumor invasion and metastasis. Although miRNA‑let‑7a (let‑7a) has been reported to suppress cell growth in multiple cancer types, the biological mechanisms of let‑7a in lung adenocarcinoma are yet to be fully elucidated. In the present study, the molecular roles of let‑7a in lung adenocarcinoma were investigated by detecting its expression in lung adenocarcinoma tissues and exploring its roles in the regulation of lung cancer cell proliferation. Let‑7a expression was identified to be downregulated in lung adenocarcinoma tissues compared with normal tissues. Overexpression of let‑7a effectively suppressed cancer cell proliferation, migration and invasion in H1299 and A549 cells. Let‑7a also induced cell apoptosis and cell cycle arrest. Furthermore, let‑7a significantly inhibited cell growth by directly regulating cyclin D1 signals. This novel regulatory mechanism of let‑7a in lung adenocarcinoma provides possible avenues for future targeted therapies of lung cancer.