Long non-coding RNA TUG1 promotes proliferation and migration in PDGF-BB-stimulated HASMCs by regulating miR-216a-3p/SMURF2 axis

BMC Molecular and Cell Biology

Xinfang Wang¹  Junsong Chen² 

[1]Department of Pediatrics, Hangzhou First People’s Hospital Affiliated to Zhejiang University, Zhejiang, Hangzhou, China

[2]Respiratory Department, Hangzhou Children’s Hospital, 195 Wenhui Road, 310003, Zhejiang, Hangzhou, China

关键词: Childhood asthma;    TUG1;    miR-216a-3p;    SMURF2;    HASMCs;   

DOI  :  10.1186/s12860-021-00396-0

来源: Springer

【 摘 要 】

BackgroundAbnormal proliferation and migration of human airway smooth muscle cells (HASMCs) play an important role in the development of childhood asthma. Long non-coding RNAs (lncRNAs) have been demonstrated to participate in HASMC proliferation and migration. We aimed to explore more effects and molecular mechanism of taurine upregulated gene 1 (TUG1) in childhood asthma.ResultsTUG1 and SMURF2 were overexpressed and miR-216a-3p was downregulated in childhood asthma patients and PDGF-BB-stimulated HASMCs. TUG1 knockdown attenuated PDGF-BB-triggered proliferation and migration of HASMCs. MiR-216a-3p was targeted by TUG1, and miR-216a-3p suppression counteracted the repressive effects of TUG1 interference on proliferation and migration in PDGF-BB-treated HASMCs. SMURF2 was a downstream target of miR-216a-3p, and SMURF2 upregulation abated the inhibiting effects of miR-216a-3p on migration and proliferation in PDGF-BB-exposed HASMCs. TUG1 sponged miR-216a-3p to positively regulate SMURF2 expression.ConclusionTUG1 downregulation inhibited PDGF-BB-induced HASMC proliferation and migration by regulating miR-216a-3p/SMURF2 axis, offering novel insight into the potential application of TUG1 for childhood asthma treatment.

【 授权许可】

CC BY