JAK2/STAT3信号对二氢杨梅素诱导骨肉瘤 MG-63细胞凋亡及其迁移的影响

Effect of JAK2/STAT3 signal on the apoptosis and migration of human osteosarcoma MG-63 cells induced by dihydrocarbamide

目的研究二氢杨梅素(dihydromyricetin,DMY)体外通过JAK2/STAT3信号通路对人骨肉瘤细胞株MG-63生长、凋亡及侵袭和迁移的影响。方法体外培养MG-63细胞,以不同浓度的DMY作用于MG-63细胞,MTT法检测不同时间和不同浓度的DMY对细胞生长的抑制作用;AnnexinV-FITC/PI双染流式细胞仪检测对细胞凋亡的影响;Transwell小室法检测细胞的侵袭和迁移能力;Western blot法检测Cyclin D1、p-JAK2、p-STAT3、Bcl-xL、Bax和Bak含量。结果 DMY可时间和浓度依赖性地抑制MG-63细胞的生长;促进MG-63细胞凋亡;抑制MG-63细胞侵袭和迁移;下调Cyclin D1、p-JAK2、p-STAT3、Bcl-xL水平,上调Bax和Bak水平(P<0.05)。结论 DMY具有抗人骨肉瘤MG-63细胞活性的作用,可降低骨肉瘤细胞侵袭和迁移能力,通过调控JAK2/STAT3信号通路抑制细胞生长,诱导细胞凋亡。

Objective To investigate the effect of dihydrocarbamide on the growth,apoptosis,invasion and migration of human osteosarcoma MG-63 cells by the PI3K/Akt signaling pathway. Methods MG-63 cells were cultured in vitro ,and MTT was performed to observe the cell proliferation after dihydrocarbamide treatment at different times. Annexin V-FITC/PI flow cytometry was used to determine the cell apoptosis rate. The cell invasion and migration were detected by Transwell method. The expression of cyclin D1, p -JAK2, p -STAT3,Bcl-xl,Bax and Bak proteins were detected by Western blot. Results Dihydrocarbamide inhibited the proliferation of MG-63 cells in vitro in a concentration- and time-dependent manner. Dihydrocarbamide promoted the cell apoptosis,and inhibited the migration and invasive ability of MG-63 cells. Additionally,dihydrocarbamide also decreased the expressions of Cyclin D1, p -JAK2, p -STAT3 and Bcl-xL,and increased the levels of Bax and Bak ( P< 0.05). Conclusion Dihydrocarbamide displays an anti-human osteosarcoma cell activity,which may be related to reduction of cell invasion,migration and growth,and induction of cell apoptosis by the JAK2/STAT3 pathway.