Our findings demonstrated that miR-203a-3p was down-regulated in asthma serums, and overexpressed miR-203a-3p inhibited TGF-β1-induced EMT in asthma by regulating Smad3 pathway through targeting SIX1, suggesting a promising therapeutic approach for bronchial epithelial cell EMT in asthma. Here, SIX1 is linked to asthma.