The dysfunction of airway smooth muscle cells (ASMCs) is one of the key factors in the pathogenesis of asthma. How miR-98-5p works in asthma has not been completely elucidated. This work focused on how miR-98-5p functions in the proliferation and migration of human ASMCs treated with interleukin-13 (IL-13). MiR-98-5p expression in plasma of asthmatic patients and IL-13-stimulated ASMCs was probed by quantitative real-time polymerase chain reaction (qRT-PCR). RAS-relevant C3 botulinum toxin substrate 1 (RAC1) protein expression in ASMCs was assessed by Western blot. The growth of ASMCs was measured by cell counting kit-8 (CCK-8) assay and 5-ethynyl-2′-deoxyuridine (EdU) assay. The migration of ASMCs was examined by Transwell assay. Besides, the apoptosis of ASMCs was analyzed by flow cytometry. The targeting relationship between miR-98-5p and RAC1 3′-UTR was verified by a dual-luciferase reporter gene assay. MiR-98-5p expression was reduced in patients’ plasma and IL-13-stimulated ASMCs, and RAC1 expression was upregulated in ASMCs treated with IL-13. MiR-98-5p overexpression inhibited IL-13-induced proliferation and migration of ASMCs while promoting the apoptosis. The opposite result was observed after inhibiting miR-98-5p expression. Besides, RAC1 was identified as a direct downstream target of miR-98-5p in ASMCs. The restoration of RAC1 expression counteracted the impacts of miR-98-5p overexpression on IL-13-stimulated proliferation, migration, and apoptosis of ASMCs. MiR-98-5p inhibits IL-13-induced proliferation and migration and accelerates the apoptosis of ASMCs by downregulating RAC1 expression.
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