MicroRNA-625 inhibits the progression of non‑small cell lung cancer by directly targeting HOXB5 and deactivating the Wnt/β-catenin pathway

Abstract

Numerous microRNAs (miRs) are dysregulated in non‑small cell lung cancer (NSCLC), serving pivotal roles in its formation and progression. miR‑625 is dysregulated in several types of human cancer, but its involvement in the formation and development of NSCLC remains poorly understood. In the present study, we aimed to investigate miR‑625 expression in NSCLC and its role in regulating NSCLC cell behavior. miR‑625 expression in NSCLC tissues and cell lines was detected using reverse transcription‑quantitative polymerase chain reaction. The effects of miR‑625 overexpression on NSCLC cell proliferation, apoptosis, migration and invasion in vitro were assessed using an MTT assay, flow cytometry, and cell migration and invasion assays, respectively. The effects of miR‑625 upregulation on NSCLC growth were evaluated in an in vivo xenograft model. The molecular mechanisms underlying the tumor‑suppressing roles of miR‑625 in NSCLC were explored in detail. miR‑625 expression was determined to be downregulated in NSCLC tissues and cell lines. This decreased expression was associated with advanced clinical features and poor overall survival of patients with NSCLC. Exogenous miR‑625 expression suppressed NSCLC cell proliferation, migration and invasion, and induced apoptosis in vitro. miR‑625 upregulation hindered NSCLC tumor growth in vivo. Homeobox B5 (HOXB5) was proposed to be the direct target gene of miR‑625 in NSCLC cells. The tumor‑suppressing effects of HOXB5 silencing were similar to those of miR‑625 overexpression in NSCLC cells. In rescue experiments, HOXB5 overexpression partially reversed the inhibitory effects of miR‑625 in NSCLC cells. miR‑625 upregulation directly targeted HOXB5 to deactivate the Wnt/β‑catenin signaling pathway in NSCLC cells in vitro and in vivo. miR‑625 was determined to be associated with HOXB5 suppression and Wnt/β‑catenin pathway deactivation, which in turn inhibited the aggressive behavior of NSCLC cells in vitro and in vivo.