β-catenin降低外源性hS100A6对骨肉瘤细胞的抑制作用

β-catenin decreases hS100A6-induced inhibition in osteosarcoma cell lines MG63 and U2OS

目的研究外源性hS100A6抑制骨肉瘤细胞作用与Wnt/β-catenin信号途径的关系。方法用携带人β-catenin及其siRNA基因的重组腺病毒Adβ-catenin和AdSiβ-catenin分别上调和下调MG63和U2OS细胞中β-catenin水平,再用重组hS100A6处理这些细胞,然后通过MTT法检测细胞增殖能力的变化,Hochest染色法检测细胞凋亡的变化,划痕愈合实验和Transwell实验检测细胞迁移能力的变化。结果①外源性hS100A6抑制2株骨肉瘤细胞的增殖(P<0.05);β-catenin过表达和低表达则分别减弱和增强hS100A6对这2株细胞的增殖抑制作用(P<0.05);②外源性hS100A6促进2株骨肉瘤细胞的凋亡(P<0.05);β-catenin过表达和低表达则分别增强和减弱hS100A6对这2株细胞的促凋亡作用(P<0.05);③外源性hS100A6抑制骨肉瘤细胞株MG63的迁移(P<0.05);β-catenin过表达和低表达则分别减弱和增强hS100A6对MG63的迁移抑制作用(P<0.05)。结论β-catenin负性调节hS100A6对骨肉瘤的抑制作用;hS100A6对骨肉瘤的抑制作用可能经由Wnt信号途径及其他信号途径共同调控。

Objective To investigate the relationship between the inhibition of hS100A6 on osteosarcoma cell lines MG63 and U2OS and Wnt/β-catenin signaling pathway.Methods Adenoviruses carrying human β-catenin and its siRNA gene respectively were used to up-regulate and down-regulate the expression of β-catenin in MG63 and U2OS cells.Then MTT assay,Hoechst staining,scratching test and Transwell assay were used to detect cells proliferation,apoptosis and migration,respectively after the treatment of hS100A6.Results Adβ-catenin and AdSiβ-catenin up-and down-regulated β-catenin expression in MG63 and U2OS （P0.05）,respectively.Exogenous hS100A6 inhibited the proliferation of wild osteosarcoma cell lines MG63 and U2OS （P0.05）,while over-or low-expression of β-catenin reduced or enhanced the inhibitive effect of S100A6 on cell proliferation respectively （P0.05）.Exogenous hS100A6 promoted the apoptosis of 2 wild cell lines （P0.05）,but over-or low-expression of β-catenin enhanced or reduced the ability of hS100A6 respectively （P0.05）.Exogenous hS100A6 inhibited the migration of MG63 cells,however,over-or low-expression of β-catenin reduced or enhanced the ability of hS100A6 to inhibit migration （P0.05）.Conclusion The inhibitory role of hS100A6 on osteosarcoma cells is regulated negatively by β-catenin.This inhibitory role may be controlled by Wnt/β-catenin and other signaling pathways.