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Rheumatoid arthritis (RA) is an autoimmune disease that occurs in approximately 1.0% of the general population. In RA patients, physical disability and joint damage are the major prognostic factors, which are associated with a reduction in the quality of life and early mortality. At present, the exact molecular mechanism of RA remains elusive. Long noncoding RNAs (lncRNAs) have been revealed to play a regulatory role in the pathogenesis of RA. To reveal the function of lncRNAs in rheumatoid arthritis, lncRNAS56464.1 was screened to verify its targeting of the microRNA (miR)‑152‑3p/Wnt pathway and its effect on the proliferation of fibroblast‑like synoviocytes (FLS). In the present study, based on the competing endogenous RNA (ceRNA) theory, siRNA was designed for transfection into FLS to calculate the lncRNAS56464.1 interference efficiency and then the effect of lncRNAS56464.1 interference on FLS proliferation was detected by MTT assay. Then, lncRNAS56464.1 targeting of the miR‑152‑3p/Wnt pathway was detected by a dual‑luciferase reporter assay. In addition, RT‑qPCR, immunofluorescence and western blotting techniques were employed to detect the expression of lncRNAS56464.1, miR‑152‑3p and some key genes of the Wnt signaling pathway in FLS after lncRNAS56464.1 interference. The results revealed that lncRNAS56464.1 could combine with miR‑152‑3p and promoted the proliferation of FLS. In addition, lncRNAS56464.1 interference could not only decrease the proliferation of FLS and the expression of Wnt1, β‑catenin, c‑Myc, cyclin D1, and p‑GSK‑3β/GSK‑3β, but it also increased the expression of SFRP4. The present data indicated that lncRNAS56464.1 could target the miR‑152‑3p/Wnt pathway to induce synovial cell proliferation and then participate in the pathogenesis of RA.

international journal of molecular medicine

lncRNAS56464.1 as a ceRNA promotes the proliferation of fibroblast‑like synoviocytes in experimental arthritis via the Wnt signaling pathway and sponges miR‑152‑3p