SNHG8/miR-873-3p/CDK6 axis triggers proliferation and migration of smooth muscle cells in intimal hyperplasia.

Aim: Long-strand non-coding RNAs play a crucial role in intimal hyperplasia. Nevertheless, the mechanism by which small nucleolar RNA host gene 8 affects intimal hyperplasia remains unknown.

Materials And Methods: The expression levels of SNHG8, miR-873-3p, and CDK6 were detected by qRT-PCR or Western blotting. Cell proliferation was measured using 5-ethynyl-2'-deoxyuridine and cell counting kit-8 assay. Cell migration was detected by Transwell and scratch assay. The binding roles and sites of miR-873-3p to SNHG8 and CDK6 were detected by dual luciferase reporter gene assay. The binding role of miR-873-3p and SNHG8 was detected by RNA immunoprecipitation assay. Vascular injury was simulated by ligation of the left common carotid artery.

Key Findings: This study suggests that the high expression of SNHG8 in intimal hyperplasia vascular smooth muscle cells can function as a competitive endogenous RNA. By specifically binding to miR-873-3p, which is weakened, SNHG8 acts as a negative regulator of CDK6 target genes, leading to upregulation of CDK6 expression. This interaction was also shown to promote vascular smooth muscle cells proliferation and migration.

Significance: This study revealed a novel regulatory mechanism of action of the SNHG8/miR-873-3p/CDK6 axis in the progression of intimal hyperplasia and points to the potential of SNHG8, miR-873-3p, and CDK6 as novel targets for the diagnosis and treatment of intimal hyperplasia.