LncRNA RMRP knockdown promotes proliferation and migration of Schwann cells by mediating the miR-766-5p/CAND1 axis.

The proliferation and migration of Schwann cells (SCs) promote nerve regeneration after facial nerve injury. In recent years, the role of long noncoding RNAs (lncRNAs) in regulating SC proliferation and migration has been gradually uncovered. However, there is little evidence on the function of lncRNA RMRP (lnc-RMRP) in SC growth. In the present study, we performed loss-of-function and overexpression assays to explore the function of lnc-RMRP in SCs. The relationships between lnc-RMRP, miR-766-5p and CAND1 (cullin-associated and neddylation-dissociated 1) were analyzed using bioinformatics analysis, luciferase detection, RNA binding protein immunoprecipitation and RNA pulldown methods. CCK-8, EdU, Transwell and wound healing assays were utilized for the detections of cell proliferation and migration. We found that lnc-RMRP silencing enhanced cell proliferation and migration of SCs, while lnc-RMRP overexpression showed the opposite effect. Mechanistically, lnc-RMRP directly bound to and negatively modulated the expression of miR-766-5p. MiR-766-5p knockdown decreased cell viability, proliferation and migration of SCs, and also reversed the effects of lnc-RMRP silencing. In addition, lnc-RMRP positively regulated CAND1 expression by sponging miR-766-5p. Upregulation of CAND1 rescued the function of lnc-RMRP knockdown in regulating SC proliferation and migration. These data suggested that lnc-RMRP played a significant role in SC proliferation and migration, indicating that lnc-RMRP might be a potential therapeutic target for the treatment of facial nerve injury.