Abstract: Abstract: Objective　To investigate the role of Linc00891 in osteosarcoma (OS) and its mechanism. Methods　The expressions of Linc00891 in different OS cell lines U-2 OS, Saos-2, MG-63, SW 1353 and human osteoblast cell line hFOB 1.19 were detected by qPCR. Saos-2 and MG-63 OS cell lines were transfected with Linc00891 vector. CCK-8 method, plate cloning method and Transwell chamber were used to detect the effects of Linc00891 overexpression on the proliferation, colony forming ability and migration ability. Western blot assay was used to detect the expressions of E-cadherin (E-cad) and N-cadherin (N-cad) related to epithelial-mesenchymal transition. RNA pulldown assay was used to detect the binding relationship between Linc00891 and miR-27a-3p in OS cells. TCF/LEF Reporter Kit was used to detect the effects of overexpression of Linc00891 and up-regulation of miR-27a-3p on Wnt/β-catenin signaling pathway in different OS cell lines. Results　The expression levels of Linc00891 in different OS cell lines U-2 OS, Saos-2, MG-63 and SW 1353 were significantly lower than those in normal osteoblast cell line hFOB 1.19 (P＜0.05). The overexpression of Linc00891 could inhibit the proliferation, clone formation, migration and epithelial mesenchymal transition of human OS cell lines Saos-2 and MG-63 (P＜0.05). There was a binding relationship between Linc00891 and miR-27a-3p in OS cells. The overexpression of Linc00891 could reverse the activation of miR-27a-3p on Wnt/β-catenin signaling pathway (P＜0.05). Conclusion　Linc00891 plays an anti-tumor role in OS by competitively binding and inhibiting miR-27a-3p.

Key words: osteosarcoma, RNA, long noncoding, genes, tumor suppressor, Wnt signaling pathway, β catenin, Linc00891, miR-27a-3p