Effects of LncRNA SNHG16 Targeting miR-425-5p on the Proliferationand Apoptosis of Synovial Fibroblasts in Rheumatoid Arthritis

This paper aimed to explore the effect of LncRNA (long non-coding RNA) SNHG16 on the proliferation and apoptosis of RA (rheumatoid arthritis) synovial fibroblasts by targeting miR-425-5p and its mechanism. The relative expression levels of SNHG16 and miR-425-5p were detected by qRT-PCR. Cell proliferation,apoptosis and the expression of Ki67 and Bax proteins were detected by CCK8, flow cytometry and Western blot,respectively. Double luciferase experiment was used to examine the targeting relationship between SNHG16 andmiR-425-5p. The relative expression of SNHG16 in RA synovial tissues and RA synovial fibroblasts was significantly increased (P<0.05), and the relative expression of miR-425-5p was significantly decreased (P<0.05). Silencing SNHG16 or overexpression of miR-425-5p significantly inhibited proliferation of RA synovial fibroblasts andpromoted cell apoptosis (P<0.05). SNHG16 can target and regulate the expression of miR-425-5p, and inhibitingmiR-425-5p can partially restore the effects of silencing SNHG16 on the proliferation and apoptosis of RA synovialfibroblasts (P<0.05). SNHG16 can inhibit the proliferation of synovial fibroblasts by up-regulating the expressionof miR-425-5p, and induce their apoptosis, providing reference data for the development of new targets for thetreatment and diagnosis of RA.

CSTR: 32200.14.cjcb.2023.11.0004