miR‑625‑5p 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 miR‑625‑5p 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 miR‑625‑5p was verified using a luciferase reporter assay. LPS was added to 16HBECs following the administration of miR‑625‑5p mimics or miR‑625‑5p inhibitors, and cells with silenced or overexpressed AKT2 levels. miR‑625‑5p was expressed at a high level in LPS‑activated 16HBECs. Overexpression of miR‑625‑5p inhibited interleukin (IL)‑6 and tumor necrosis factor (TNF)‑α secretion in 16HBECs. Inhibition of miR‑625‑5p enhanced LPS‑induced IL‑6 and TNF‑α secretion. miR‑625‑5p negatively regulated the expression of AKT2 in 16HBECs. A dual‑luciferase reporter assay system confirmed that miR‑625‑5p directly targeted the 3'untranslated region of AKT2. Transfection with a small interfering RNA against AKT2 inhibited inhibitor of κB phosphorylation. In brief, miR‑625‑5p may protect LPS‑induced HBECs by targeting AKT2 and inhibiting the nuclear factor‑κB signaling pathway. Therefore, miR‑625‑5p may function as an inhibitor of asthma airway inflammation in HBECs by targeting AKT2.