MiR‑379 inhibits cell proliferation and epithelial‑mesenchymal transition by targeting CHUK through the NF‑κB pathway in non‑small cell lung cancer

Abstract

An increasing body of evidence has demonstrated that microRNA (miR) deregulation serves pivotal roles in tumor progression and metastasis. However, the function of miR-379 in lung cancer remains understudied, particularly in non-small cell lung cancer (NSCLC). Bioinformatics and luciferase reporter analyses confirmed that conserved helix-loop-helix ubiquitous kinase (CHUK) is a target of miR-379, which may directly bind to the 3'-untranslated region of CHUK and significantly downregulate its expression in NSCLC cells. Transwell assays were used to evaluate the role of miR-379 in cell migration and invasion, and western blotting was used to address the association between miR-379 and epithelial-mesenchymal markers, including E-cadherin, cytokeratin and Vimentin. In the present study, miR-379 expression in NSCLC tissues and cell lines was downregulated, which may be associated with the poor survival of patients with NSCLC. miR-379 may act as a tumor suppressor in NSCLC, potentially by suppressing cell growth and proliferation, delaying G1-S transition, enhancing cell apoptosis and suppressing NSCLC cell migration and invasion. Furthermore, it was also observed that CHUK may function as an oncogene, and downregulation of CHUK induced by miR-379 may partially rescue the malignant characteristics of tumors, indicating that miR-379 may be suppressed in tumorigenesis. The overexpression of miR-379 may prevent the growth of NSCLC tumors via CHUK suppression and the downstream nuclear factor-κB pathway. The results of the present study demonstrated that miR-379 may act as a tumor suppressor, and may constitute a potential biomarker and a promising therapeutic agent for the treatment for NSCLC.