LncRNA PART-1 targets TGFBR2/Smad3 to regulate cell viability and apoptosis of chondrocytes via acting as miR-590-3p sponge in osteoarthritis

Osteoarthritis (OA) is a degenerative joint disease that commonly occurs in the elderly. This study focused on apoptosis and explored the modulating effects of long non-coding (lncRNAs) prostate androgen-regulated transcript-1 (PART-1) on chondrocytes apoptosis. In the present study, the PART-1 expression level was down-regulated in the OA cartilages. Silence of PART-1 decreased the cell viability and promoted chondrocytes apoptosis. Overexpression of PART-1 could reverse the effects induced by interleukin 1 beta (IL-1 beta) stimulation, thus slowing down the apoptosis rate. MiR-590-3p was found to be the potential target, and RNA immunoprecipitation and luciferase activity assay confirmed the binding between PART-1 and miR-590-3p. Moreover, miR-590-3p was down-regulated by PART-1 and was negatively associated with PART-1. Transforming growth factor-beta receptor type 2 (TGFBR2) was positively associated with PART-1. Down-regulation of PART-1 decreased cell viability and induced cell apoptosis, which was partially reversed by miR-590-3p silence or TGFBR2 overexpression; while overexpression of PART-1 increased the cell viability and decreased the caspase 3 activity and apoptotic rates, and the effects were partially attenuated by miR-590-3p overexpression or silence of TGFBR2 in IL-1 beta-stimulated chondrocytes. Knock-down of PART-1 down-regulated both Smad3 and p-Smad3 protein levels, which was reversed by miR-590-3p inhibition or TGFBR2 overexpression. Smad3 expression level was lower in the OA group than that in the normal group and was positively associated with the PART-1 expression level. Collectively, the study revealed that lncRNA PART-1 regulates the apoptosis of chondrocytes in OA by acting as a sponge for miR-590-3p, which subsequently regulates TGFBR2/Smad3 signalling.