Abstract
Osteoarthritis (OA) acts as the most common type of degenerative joint disease. Long noncoding RNA (lncRNA) has been identified to regulate the apoptosis and proliferation of chondrocyte. However, the deepgoing mechanism involved in the regulation is still unclear. This research aims to investigate the role and molecular mechanism by which lncRNA LINC00511 regulates the OA biology. Functionally, the functional experiments found that LINC00511 expression was upregulated in the IL-1β–stimulated chondrocyte (ATDC5). Knockdown of LINC00511 facilitated proliferation, and repressed the apoptosis and extracellular matrix (ECM) synthesis of chondrocyte. Mechanically, LINC00511 functioned as sponge of miR-150-5p and then interacted with the 3′-UTR of transcription factor (SP1). In turn, transcription factor SP1 bound with the promoter region of LINC00511 and thus upregulated LINC00511 expression. In conclusion, our findings highlight the function and prognostic value of LINC00511/miR-150-5p/SP1 feedback loop in OA and extend the importance of lncRNA epigenetics in OA biology.
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