LncRNA LINC-PINT increases SOCS1 expression by sponging miR-155-5p to inhibit the activation of ERK signaling pathway in rheumatoid arthritis synovial fibroblasts induced by TNF-α

Rheumatoid arthritis (RA) is a systemic and chronic autoimmune disease associated with altered gene expression in synovial tissue. Long intergenic non-protein encoding long-chain RNA p53-induced transcript (LncRNA LINC-PINT) has been reported to be involved in multiple physiological and pathological processes. However, the role of lncRNA LINC-PINT in RA is rarely mentioned. To investigate the mechanism of LINC-PINT in RA, we constructed a RA model using TNF-alpha-induced method to explore the downstream effector and signaling pathway. We found that LINC-PINT was downregulated in RA tissues and TNF-alpha stimulated RA cells. And overexpression of LINC-PINT could inhibit cell proliferation and invasion induced by TNF-alpha through downregulating the levels of IL-1 beta and MMPs and inhibiting the activation of ERK pathway. Using bioinformatics analysis and RNA Binding Protein Immunoprecipitation (RIP) assay, we verified that LINC-PINT directly interacted with miR-155-5p, and miR-155-5p could regulate the expression of SOCS1. Whereas, downregulation of miR-155-5p inhibited cell growth and invasion. Overexpression of miR-155-5p could reverse the inhibitory effect of LINC-PINT induced by TNF-alpha. Furthermore, silencing SOCS1 promoted cell proliferation and invasion, upregulated the expression of IL-1 beta and MMPs, and activated ERK pathway, while overexpression of LINC-PINT could reverse the control of knocking down SOCS1. In conclusion, we revealed that LINC-PINT suppressed TNF-alpha induced cell proliferation and invasion which might be induced through downregulating miR-155-5p, influencing the expression of SOCS1, IL-1 beta and MMPs and inactivating ERK signaling pathway.