MicroRNA-29c inhibits proliferation and promotes apoptosis in non-small cell lung cancer cells by targeting VEGFA.

Abstract

Non-small cell lung cancer (NSCLC) is a primary sub-type of lung cancer with a high incidence rate and poor prognosis. The primary therapeutic treatment for NSCLC is chemotherapy, which is considered to be ineffective and excessively toxic. Novel therapeutic methods, particularly molecular targeted therapy, have attracted considerable attention. MicroRNAs (miRs) are reported to be potential biomarkers and targeted agents with roles in various types of tumors. Herein, the present study presented the observation of aberrant low expression of miR‑29c and associated overexpression of vascular endothelial growth factorA (VEGFA) in NSCLC tumor tissues. The effects of miR‑29c upon NSCLC tumor progression, including cell proliferation and cellular apoptosis, were investigated. The possible regulatory mechanism of action of miR‑29c on its direct target VEGFA and the phosphatidylinositol 3‑kinase (PI3K)/RAC‑α serine/threonine‑protein kinase (Akt) signaling pathway was examined using multiple methods, including reverse transcription-quantitative polymerase chain reaction analysis, dual luciferase assay and western blot analysis. The results demonstrated that miR‑29c expression was downregulated in NSCLC tumor tissues compared with normal tissues. A marked negative correlation in the expression of miR‑29c and VEGFA was observed in clinical NSCLC tissues and cultured NSCLC cells. Overexpression of miR‑29c may inhibit cell proliferation and accelerate the cellular apoptosis rate of NSCLC tumor cells. Furthermore, the overexpression of miR‑29c was demonstrated to be able to downregulate the expression levels of VEGFA and PI3K/Akt signaling pathway‑associated proteins. The results of the present study suggested that miR‑29c might regulate NSCLC tumor progression by targeting VEGFA.