Tectorigenin regulates migration, invasion, and apoptosis in dexamethasone-induced human airway epithelial cells through up-regulating miR-222-3p

Glucocorticoids (GCs) can effectively control airway inflammation, but can also cause airway epithelial injury. Tectorigenin, a type of isoflavone isolated from various medicinal plants, has hypolipidemic activity, hepatoprotective, and antioxidant effects. We aimed to investigate whether Tectorigenin can repair GCs-induced airway epithelial injury. Airway epithelial cell line (9HTE cells) were treated with dexamethasone (Dex), Tectorigenin, or further transfected, then cell viability, migration, and invasion were examined by Cell Counting Kit (CCK-8), wound healing, and Transwell assays. The expressions of potential miRNAs related to the effect of Tectorigenin were detected by quantitative polymerase chain reaction (qPCR). Expressions of poptosis-related proteins Bcl-2-associated protein-X (Bax), B-cell lymphoma-2 (Bcl-2), Cleaved Caspase-3, and related to Mitorgen-activated protein kinase (MAPK) signaling pathway serine/threonine kinase (Raf1), extracellular signal-regulated kinase kinase 1/2 (MEK1/2), and extracellular signal-regulated kinase 1/2 (ERK1/2) were detected by Western blot. Dex inhibited the cell viability, migration and invasion by promoting Bax and Cleaved Caspase-3 expressions (p <.001) and by inhibiting the expressions of Bcl-2 and miR-222-3p (p <.001). Then, 10 μmol/L Tectorigenin itself did not affect cell viability but could inhibit the effect of Dex on cell viability, migration, and invasion. Tectorigenin up-regulated the expressions of miR-222-3p, Bcl-2, p-Raf1, p-MEK1/2, and p-ERK1/2 (p <.01), but down-regulated the expressions of Bax and Cleaved Caspase-3 (p <.05) in Dex-induced cells. MiR-222-3p inhibitor reversed the antagonistic effect of Tectorigenin on Dex. The study demonstrates that Tectorigenin inhibits apoptosis of Dex-induced 9HTE cells by up-regulating the expression of miR-222-3p, which involves with the MAPK pathway.