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

In accordance with increasing studies, long non-coding RNAs (LncRNAs) act pivotally in the occurrence as well as development of several human diseases. But how lncRNA SNHG12 acts in osteoarthritis (OA) is still not clear.

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.

The inflammatory factor IL-1β induced chondrocytes to express lncRNA SNHG12, and lncRNA SNHG12 expression was up-regulated in OA tissues. Additionally, our personnel proved that IL-1β inhibited miR-16-5p expression 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 revealed that miR-16-5p is a target of lncRNA SNHG12.

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.