LncRNA SNHG16 promotes Schwann cell proliferation and migration to repair sciatic nerve injury

Background: To investigate the expression of long non-coding RNA (lncRNA) Snorna hostgene16 (SNHG16) in sciatic nerve injury tissues and cells. The molecular mechanism of SNHG16 regulating signal activator of transcription 3 (STAT3) expression through "sponge" adsorption of miR-93-5p was also studied. Methods: A rat model of sciatic nerve injury was established, and primary Schwann cells (SCs) were extracted. The expression of SNHG16 in animal tissues with sciatic nerve injury and SCs treated with ischemia and hypoxia was detected by qPCR, and CCK-8 assay, cell scratch assay, and Transwell chamber assay were used to detect cell proliferation, migration, and invasion. The targeted binding of SNHG16 to miR-93-5p was verified by double luciferase reporter gene assay and miRNA immunoprecipitation assay. MiR-93-5p mimic, SNHG16 overexpression vector, and sh-STAT3 plasmid were transfected into cells, respectively, and the mRNA expressions of SNHG16, miR-93-5p, and STAT3 in the cells were detected by qPCR. Results: The expression of lncRNA SNHG16 was decreased after sciatic nerve injury, while overexpression of SNHG16 promoted the proliferation, migration, and invasion of SCs. The results of dual luciferase reporter gene assay and miRNA immunoprecipitation reaction showed miR-93-5p interacted with SNHG16, and the overexpression of miR-93-5p reversed the promoting effects of SNHG16 on the proliferation and invasion of SCs. At the same time, the knockdown of STAT3, which is the target gene of miR-93-5p, reversed the proliferation and invasion promotion effect of SNHG16 on SCs. SNHG16 affected the expression of its downstream target gene STAT3 by adsorbing miR-93-5p via endogenous competitive sponge. Conclusions: SNHG16 can regulate STAT3 expression by sponge adsorption of miR-93-5p in SCs, and SNHG16 and miR-93-5p can be used as potential targets for the diagnosis and treatment of sciatic nerve injury.