MALAT1 enhanced the proliferation of human osteoblasts treated with ultrahigh molecular weight polyethylene by targeting VEGF via miR225p

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 metastasisassociated 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 ultrahigh 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 osteolysisassociated signaling were also examined, and the interactions that occurred between MALAT1 and an antiosteolysis molecule, microRNA (miR)225p were investigated. Additionally, knockdown of vascular endothelial growth factor (VEGF) exerted similar biological effects as observed following miR225p overexpression. The data showed that MALAT1 and proosteolysis indicators, receptor activator of nuclear factorκB ligand (RANKL) and VEGF were upregulated in clinical interface membrane samples. Knockdown of MALAT1 inhibited the growth of UHMWPEtreated 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 miR225p, and also between MALAT1 and miR225p. Additionally, subsequent assays indicated that overexpression of MALAT1 suppressed the antiosteolysis effect of miR225p, 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 miR225p.