miR­625­5p suppresses inflammatory responses by targeting AKT2 in human bronchial epithelial cells.

Asthma is a common chronic inflammatory airway disease; however, whether microRNAs (miRs) could be used in the treatment of asthma remains unclear. The aim of the present study was to investigate the role of miR­625­5p in the inflammatory response of human bronchial epithelial cells (HBECs). Inflammation in the HBEC line, 16HBEC, was induced using different concentrations of lipopolysaccharide (LPS), which demonstrated that 1 µg/ml LPS was an appropriate concentration for further experiments. The association between protein kinase B2 (AKT2) and miR­625­5p was verified using a luciferase reporter assay. LPS was added to 16HBECs following the administration of miR­625­5p mimics or miR­625­5p inhibitors, and cells with silenced or overexpressed AKT2 levels. miR­625­5p was expressed at a high level in LPS­activated 16HBECs. Overexpression of miR­625­5p inhibited interleukin (IL)­6 and tumor necrosis factor (TNF)­α secretion in 16HBECs. Inhibition of miR­625­5p enhanced LPS­induced IL­6 and TNF­α secretion. miR­625­5p negatively regulated the expression of AKT2 in 16HBECs. A dual­luciferase reporter assay system confirmed that miR­625­5p directly targeted the 3'untranslated region of AKT2. Transfection with a small interfering RNA against AKT2 inhibited inhibitor of κB phosphorylation. In brief, miR­625­5p may protect LPS­induced HBECs by targeting AKT2 and inhibiting the nuclear factor­κB signaling pathway. Therefore, miR­625­5p may function as an inhibitor of asthma airway inflammation in HBECs by targeting AKT2.