Mechanistic insights into lncRNA SNHG6 during the progression of osteoarthritis

The present study investigated the role and preliminary regulatory mechanism of the long non-coding RNA small nucleolar RNA host gene 6 (SNHG6) in lipopolysaccharide (LPS)-induced chondrocytes.LPS-induced chondrocytes were used to mimic osteoarthritis (OA) in vitro.Gain-and loss-of-function experiments were performed as follows: the Cell Counting Kit-8 assay for cell viability, flow cytometry for cell cycle and apoptosis analysis, the TUNEL assay for further apoptosis detection, western blotting for apoptosis-and cell cycle-related protein levels, and ELISA for inflammatory cytokine levels.Gene expression levels were detected by reverse transcription-quantitative PCR and immunofluorescence.In LPS-induced chondrocytes and in patients with OA, reduced expression of SNHG6 and PGAP1 as well as increase expression of microRNA (miR)-944 were observed.SNHG6 targets miR-944, and PGAP1 is a target of miR-944.Overexpression of SNHG6 or PGAP1, as well as downregulation of miR-944 markedly suppressed chondrocyte apoptosis and inflammation.Furthermore, increased miR-944 expression reversed the regulatory effects of PGAP1 overexpression in LPS-induced chondrocytes.In conclusion, the role and underlying mechanism of SNHG6 in the progression of OA in vitro were preliminarily identified, and it was found that its overexpression remarkably inhibits chondrocyte apoptosis and inflammation.This regulatory effect may be mediated by regulating the miR-944/PGAP1 axis.