LncRNA SNHG12 Promotes Osteoarthritis Progression Through Targeted Down-Regulation of miR-16-5p

Background: In accordance with increasing studies, long non-coding RNAs (LncRNAs) act pivotally in the occur-rence as well as development of several human diseases. But how lncRNA SNHG12 acts in osteoarthritis (OA) is still not clear. Methods: We applied CCK-8 to determine cell viability, along with qRT-PCR to detect mRNA expression. Using luciferase reporter experiment, our team detected the binding relationship between lncRNA SNHG12 along with miR-16-5p. Results: The inflammatory factor IL-1 beta induced chondrocytes to express lncRNA SNHG12, and lncRNA SNHG12 expression was up-regulated in OA tissues. Additionally, our personnel proved that IL-1 beta inhibited miR-16-5p ex-pression in chondrocytes, which in OA tissues was lower than that in normal tissues. miR-16-5p expression level in the OA patients' tissue was negatively correlated with lncRNA SNHG12 expression. The high-expression lncRNA SNHG12 inhibits chondrocyte proliferation, promoting apoptosis and inflammation as well as extracellular matrix (ECM) degradation. These effects can be reversed by co-transfecting miR-16-5p mimic. In addition, our work re-vealed that miR-16-5p is a target of lncRNA SNHG12. Conclusions: lncRNA SNHG12 regulates OA development by inhibiting miR-16-5p expression in chondrocytes. We believe that the lncRNA SNHG12/miR-16-5p axis might be a potential therapeutic and diagnostic target for OA.

Automated summary

LncRNA SNHG12 regulates the development of osteoarthritis (OA) by inhibiting miR-16-5p expression in chondrocytes, potentially serving as a therapeutic and diagnostic target for OA.