Overexpressed LINC01510 Attenuates Epithelial-Mesenchymal Transition in High Glucose-Induced Renal Tubular Epithelial Cells via Inactivating MMP7

Objective. Matrix metallopeptidase 7 (MMP7) can promote renal fibrosis in diabetic kidney disease (DKD). A study found that LINC01510 overexpression inhibits MMP7 to play a role in renal cancer, but the relationship between the two in DKD had not been revealed, and the function of LINC01510 also needed to be explored, which was also the focus of this study. Methods. The morphological changes of HK-2 cells induced by high glucose were observed by an inverted microscope, and fluorescence in situ hybridization was used to determine the subcellular localization of LINC01510. Quantitative real-time polymerase chain reaction was used to detect the levels of LINC01510 and MMP7. The effect of LINC01510 and MMP7 overexpression on high glucose-induced HK-2 cell migration and epithelial-mesenchymal transition (EMT)-related protein changes was confirmed by wound healing experiments and western blot. Results. High glucose induced HK-2 cells to gradually lose their epithelial phenotype, and decreased LINC01510 in a time-dependent manner. LINC01510 was located in the nucleus of HK-2 cells. LINC01510 overexpression increased the level of LINC01510, inhibited cell migration, and reduced the expression of MMP-7, Vimentin, alpha-SMA, and Fibronectin protein, and promoted the expression of E-cadherin protein in high glucose-induced cells. The effect of MMP7 overexpression on migration and EMT-related proteins was opposite to the effect of LINC01510 overexpression, and partially reversed the effect of LINC01510 overexpression in high glucose-induced cells. Conclusion. Our research shows that LINC01510 overexpression inactivates MMP7 to attenuate high glucose-induced EMT of renal tubular epithelial cells.