MicroRNA-379 acts as a tumor suppressor in non-small cell lung cancer by targeting the IGF‑1R-mediated AKT and ERK pathways.

Lung cancer is one of the most common types of malignancy in humans and is a leading cause of cancer-related deaths among men and women worldwide. Aberrantly expressed microRNAs in non-small cell lung cancer (NSCLC) contribute to tumor occurrence and development as either tumor suppressors or promoters. MicroRNA-379 (miR‑379) is dysregulated in several types of human cancer. However, its expression pattern, role and underlying mechanism in NSCLC progression and metastasis are poorly understood. In this study, assay of reverse transcription-quantitative polymerase chain reaction showed that miR‑379 was downregulated in both NSCLC tissue and cell lines. Low miR‑379 expression in NSCLC tissues was significantly correlated with TNM stage and lymph node metastasis. In addition, functional experiments revealed that restoring the expression of miR‑379 inhibited cell proliferation, migration and invasion of NSCLC. The insulin-like growth factor receptor-1 (IGF‑1R) was identified as a direct target of miR‑379 in NSCLC. IGF‑1R was highly expressed in NSCLC tissues and inversely correlated with miR‑379 expression. Downregulation of IGF‑1R had tumor suppressive roles similar to that of miR‑379 overexpression on NSCLC cell proliferation, migration and invasion. Moreover, the upregulation of IGF‑1R effectively rescued the tumor suppressive roles induced by miR‑379 overexpression in NSCLC. The resumption of the expression of miR‑379 inhibited the activation of AKT and ERK signaling pathways in NSCLC. These findings suggested that miR‑379 acts as a tumor suppressor in NSCLC by directly targeting IGF‑1R and indirectly regulating AKT and ERK signaling pathways. miR‑379 provides novel therapeutic targets for the treatment of patients with this disease.