Cigarette smoke promotes chronic obstructive pulmonary disease (COPD) through the miR-130a/Wnt1 axis.

Cigarette smoke (CS) is a crucial factor in chronic obstructive pulmonary disease (COPD). Wnt/β-catenin signaling deregulation may further contribute to COPD progression. The deregulation and dysfunction of miRNAs in COPD have been reported. Investigating the deregulated miRNAs and their potential role in COPD progression may provide novel strategies for COPD treatment. In the present study, we analyzed significantly differentially-expressed miRNAs in COPD according to GSE44531 and miR-130a was selected. We revealed the upregulation of miR-130a in COPD, both in cigarette smoke extract (CSE)-treated BEAS-2B cells and CS-exposed mice. MiR-130a negatively regulated three critical factors in Wnt/β-catenin signaling, Wnt1, β-Catenin, and LEF1. MiR-130a inhibition rescued CSE-blocked activation of Wnt/β-catenin signaling in vitro. MiR-130a targets WNT1 3'UTR to inhibit its expression. Moreover, in CSE-stimulated BEAS-2B cells, miR-130a overexpression aggravated, while miR-130a inhibition partially attenuated CSE-caused suppression on cell migration and proliferation. MiR-130a aggravates CSE-induced cellular injury in BEAS-2B cells by targeting Wnt signaling. In summary, miR-130a has a pathogenetic role in CS-induced COPD and regulates Wnt/β-catenin signaling via targeting Wnt1. Our findings indicate that miR-130a is a potential therapeutic target for the treatment of CS-induced COPD.