Conclusion
NEAT1 knockdown inhibited myofibroblast activities and Wnt/β-catenin pathway via miR-760/TPM1 axis in fBMFs. NEAT1 could be the target for inhibiting myofibroblast activities in fBMFs for OSF treatment.
Methods
Fibrous buccal mucosa fibroblasts (fBMFs) were from OSF specimens. Myofibroblast activities including the alpha smooth muscle actin (α-SMA) distribution and invasion capacities were determined by Immunocytochemistry and Transwell assays. Gene and protein were identified by quantitative real time polymerase chain reaction or western blotting. Binding relationship was analyzed via Starbase and dual-luciferase reporter or RNA immunoprecipitation assays.
Purpose
Oral submucous fibrosis (OSF) is a fibrotic disease with high transformation of malignant disorders. Aberrant expression of lncRNA nuclear enriched abundant transcript 1 (NEAT1) was engaged with various fibrosis models, but its mechanism in OSF remained elusive. Materials and
Results
NEAT1 and Tropomyosin-1 (TPM1) were significantly increased in OSF specimens, but miR-760 was decreased. NEAT1 knockdown repressed myofibroblast activities and reduced the fibrosis and Wnt/β-catenin pathway via miR-760/TPM1 axis. MiR-760 inhibition could reverse the regulation of NEAT1 knockdown via TPM1 in fBMFs.