MiR‑150 promotes the proliferation and migration of non‑small cell lung cancer cells by regulating the SIRT2/JMJD2A signaling pathway.

Abstract

Lung cancer (LC), as the most common cause of cancer‑related mortality worldwide, is characterized by difficulties in early detection, a high degree of malignancy, poor sensitivity to radiotherapy and chemotherapy, and a low 5‑year survival rate. MicroRNA (miRNA) is a class of small, non‑coding, endogenously expressed RNA that serves vital roles in RNA silencing and post‑transcriptional regulation of gene expression. Previous studies have shown that abnormal expression of miRNA is relevant to various malignant tumors, including lung cancer. In the present study, miR‑150 was found to be significantly upregulated in non‑small cell lung cancer (NSCLC) cells, which also exhibited downregulation of SIRT2. Through downregulation of miR‑150 and/or overexpression of SIRT2 in NSCLC cells (A549 and H1299), invivo assays revealed that the suppression of miR‑150 and re‑expression of SIRT2 could inhibit NSCLC cell growth. Additionally, the present data demonstrated that miR‑150 regulated NSCLC cell viability and mobility through SIRT2/JMJD2A. Finally, it was demonstrated that silencing of miR‑150 led to inactivation of the AKT signaling pathway, which eventually inhibited the viability and mobility of NSCLC cells. This inhibitory effect of miR‑150 could be exacerbated by upregulation of SIRT2. In conclusion, our results demonstrated that miR‑150 plays an important role in the development of lung cancer by serving as an oncogene via the SIRT2/JMJD2A signaling pathway.