Silencing lncRNA MALAT1 can promote autophagy and migration of C28/I2 chondrocytes induced by nitroprusside

Abstract

Abstract Objective: To explore the effect of metastasis-associated lung adenocarcinoma transcript (MALAT1) on the autophagy, migration ability and cell survival rate of C28/I2 chondrocytes induced by sodium nitroprusside (SNP). Methods: C28/I2 chondrocytes were treated with 0 mM, 0.5 mM, 0.75 mM, and 1 mM SNP for 12 h; si-MALAT1 was introduced into C28/I2 chondrocytes by lipofection technology followed by treatment and SNP for 12 h. The cell survival rate was measured using the CCK-8 method ,and cell migration was observed through cell scratch assays.The expression levels of autophagy-related proteins was measured using western blotting.The expression level of the MALAT1 gene was verified through qRT-PCR experiments. The effects of different concentrations of SNP on autophagy in C28/I2 chondrocytes were observed using mono-dansyl cadaverine (montane sulfonyl cadaverine, MDC) staining under a fluorescence microscope. Results: The results showed that the expression level of Beclin-1andATG5, cell migration rate, and cell survival rate all decreased significantly,The lowest expression level was observed in cells cultured with 1 mM SNP concentration; The formation of autophagosomes was minimal when cells were cultured at 1 mM SNP concentration by fluorescence microscopy. The expression level of the MALAT1 gene was significantly increased in C28/I2 chondrocytes treated with 1 mM SNP for 12 h. Silencing MALAT1 led to up-regulation of the expression levels of two autophagy-related proteins, ATG5 and Beclin-1 in C28/I2 chondrocytes induced by SNP, resulting in increased cell migration and cell survival. Conclusion: SNP can inhibit the autophagy, cell migration ability and survival rate of C28/I2 chondrocytes. MALAT1 plays an important role in developing osteoarthritis (OA) by affecting SNP-induced autophagy, migration ability, and cell survival rate in C28/I2 chondrocytes. Therefore, MALAT1 could be a potential target for osteoarthritis treatment.