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.

中文翻译：

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正反馈回路LINC00511 / miR-150-5p / SP1调节骨关节炎中的软骨细胞凋亡和增殖。

骨关节炎（OA）是变性关节疾病的最常见类型。长非编码RNA（lncRNA）已被确定来调节软骨细胞的凋亡和增殖。但是，该法规涉及的深层机制仍不清楚。这项研究旨在研究lncRNA LINC00511调控OA生物学的作用和分子机制。在功能上，功能实验发现LINC00511在IL-1β刺激的软骨细胞（ATDC5）中表达上调。敲低LINC00511促进增殖，并抑制软骨细胞的凋亡和细胞外基质（ECM）合成。在机械上，LINC00511充当miR-150-5p的海绵，然后与转录因子（SP1）的3'-UTR相互作用。反过来，转录因子SP1与LINC00511的启动子区域结合，从而上调LINC00511的表达。总之，我们的发现突出了LINC00511 / miR-150-5p / SP1反馈环在OA中的功能和预后价值，并扩展了lncRNA表观遗传学在OA生物学中的重要性。