[No authors listed]
Numerous microRNAs (miRs) are dysregulated in nonâsmall cell lung cancer (NSCLC), serving pivotal roles in its formation and progression. miRâ625 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 miRâ625 expression in NSCLC and its role in regulating NSCLC cell behavior. miRâ625 expression in NSCLC tissues and cell lines was detected using reverse transcriptionâquantitative polymerase chain reaction. The effects of miRâ625 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 miRâ625 upregulation on NSCLC growth were evaluated in an in vivo xenograft model. The molecular mechanisms underlying the tumorâsuppressing roles of miRâ625 in NSCLC were explored in detail. miRâ625 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 miRâ625 expression suppressed NSCLC cell proliferation, migration and invasion, and induced apoptosis in vitro. miRâ625 upregulation hindered NSCLC tumor growth in vivo. Homeobox B5 (HOXB5) was proposed to be the direct target gene of miRâ625 in NSCLC cells. The tumorâsuppressing effects of HOXB5 silencing were similar to those of miRâ625 overexpression in NSCLC cells. In rescue experiments, HOXB5 overexpression partially reversed the inhibitory effects of miRâ625 in NSCLC cells. miRâ625 upregulation directly targeted HOXB5 to deactivate the Wnt/βâcatenin signaling pathway in NSCLC cells in vitro and in vivo. miRâ625 was determined to be associated with HOXB5 suppression and Wnt/βâcatenin pathway deactivation, which in turn inhibited the aggressive behavior of NSCLC cells in vitro and in vivo.
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