MALAT1 enhanced the proliferation of human osteoblasts treated with ultra-high molecular weight polyethylene by targeting VEGF via miR-22-5p

Osteolysis associated with an implanted prosthesis is the major cause of failure in prosthesis implantation, and a severe public health issue worldwide. The type of bone metabolism associated with this disorder has been a major focus for improving the outcomes of patients with osteolysis. The role of metastasis-associated lung adenocarcinoma transcript 1 (MALAT1; a member of the long coding RNA family) during the onset of osteolysis and the related molecular regulatory mechanism in ultra-high molecular weight polyethylene (UHMWPE)-treated hFOB 1.19 cells were investigated in the current study. The effect of MALAT1 knockdown on cell viability, cell apoptosis and osteolysis-associated signaling were also examined, and the interactions that occurred between MALAT1 and an anti-osteolysis molecule, microRNA (miR)-22-5p were investigated. Additionally, knockdown of vascular endothelial growth factor (VEGF) exerted similar biological effects as observed following miR-22-5p overexpression. The data showed that MALAT1 and pro-osteolysis indicators, receptor activator of nuclear factor-kappa B ligand (RANKL) and VEGF were upregulated in clinical interface membrane samples. Knockdown of MALAT1 inhibited the growth of UHMWPE-treated hFOB 1.19 cells, and this effect was associated with the upregulation of OPG, and downregulation of RANKL and VEGF. Results of a dual luciferase assay confirmed the interaction between VEGF and miR-22-5p, and also between MALAT1 and miR-22-5p. Additionally, subsequent assays indicated that overexpression of MALAT1 suppressed the anti-osteolysis effect of miR-22-5p, which would further induce VEGF expression. The data indicated that MALAT1 has an in port ant role in the onset of osteolysis via its ability to induce RANKL expression and inhibit the effect of miR-22-5p.