miR‑29a‑3p inhibits the malignant characteristics of non‑small cell lung cancer cells by reducing the activity of the Wnt/β‑catenin signaling pathway
Kang Zhang, Xiaoliang Han, Wenbin Hu, Chao Su, Binjun He
Abstract
MicroRNAs (miRNAs) can influence non‑small cell lung cancer (NSCLC) in a tumor‑suppressive and oncogenic manner. The present study aimed to investigate the effects and underlying mechanisms of miR‑29a‑3p in NSCLC. NSCLC cell lines (A549, H1299, and H460) and a normal lung epithelial cell line (BEAS‑2B) were used. Additionally, a mouse lung tumor xenograft model was established using A549 cells and used to determine the effects of miR‑29a‑3p on NSCLC <em>in vivo</em>. Tumor volumes were measured every week. The expression of miR‑29a‑3p in cells and lung tissues were detected by RT‑qPCR. Cell proliferation was detected using Cell Counting Kit‑8 and EdU assays. Migration and invasion were assessed using wound healing and Transwell invasion assays, respectively. Ki‑67 expression was detected using immunohistochemical staining. The expression levels of Wnt3a and β‑catenin were determined using western blotting. miR‑29a‑3p expression was significantly downregulated in NSCLC cells and mice. In contrast to miR‑29a‑3p knockdown, miR‑29a‑3p overexpression decreased NSCLC cell proliferation, migration, and invasion as well as tumor growth in in the NSCLC mouse model. Moreover, miR‑29a‑3p overexpression decreased the protein expression levels of Wnt3a and β‑catenin. The inhibitory effects of miR‑29a‑3p on NSCLC cells were reversed by LiCl (an activator of the Wnt signaling pathway). In conclusion, miR‑29a‑3p prevented NSCLC tumor growth and cell proliferation, migration, and invasion by inhibiting the Wnt/β‑catenin signaling pathway. This finding offers novel insights into the prognosis and treatment of NSCLC.