Journal
BMC MOLECULAR AND CELL BIOLOGY
Volume 22, Issue 1, Pages -Publisher
BMC
DOI: 10.1186/s12860-021-00396-0
Keywords
Childhood asthma; TUG1; miR-216a-3p; SMURF2; HASMCs
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The study revealed that TUG1 is overexpressed in childhood asthma patients and PDGF-BB-stimulated HASMCs, and it inhibits HASMC proliferation and migration induced by PDGF-BB by regulating the miR-216a-3p/SMURF2 axis.
Background Abnormal 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. Results TUG1 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. Conclusion TUG1 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.
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