紫铆因对骨肉瘤细胞凋亡和转移的影响及其机制

The mechanism of Butein in promoting apoptosis and inhibiting metastasis of osteosarcoma cells

目的:研究不同浓度的紫铆因对U2OS骨肉瘤细胞的凋亡及侵袭转移作用的影响,并探讨其相关的作用机制。方法:U2OS骨肉瘤细胞在不同浓度的紫铆因作用下处理24 h,CCK-8细胞活性试剂盒测定U2OS骨肉瘤细胞活性的变化;Western blot法测定U2OS骨肉瘤细胞中凋亡相关蛋白Bax、Bcl-2,侵袭转移相关蛋白MMP-2、MMP-9,PI3K-Akt细胞信号通路相关蛋白的表达情况;Tunel法检测U2OS细胞的凋亡情况。结果:25、50、100μmol/L紫铆因处理组与0μmol/L紫铆因组比,细胞活性差异均有统计学意义(P<0.05);50、100μmol/L紫铆因处理组与0μmol/L紫铆因组比,Bax的表达量增加,Bcl-2、MMP-2、MMP-9表达量降低,PI3K-Akt信号通路相关蛋白表达量下降,差异均有统计学意义(P<0.05)。结论:紫铆因可以促进U2OS骨肉瘤的凋亡并抑制其侵袭转移,这种作用可能是通过抑制PI3K-Akt信号通路来实现的。

Objective:To study the effects of Butein on apoptosis and invasion and metastasis of U2OS osteosarcoma cells.Methods:U2OS osteosarcoma cells were treated with different doses of Butein for 24 h respectively.CCK-8 assay was used to detect the activity of U2OS cells.Western blot assay was used to detect the expression of Bcl-2,Bax,MMP-2,MMP-9,and the PI3K-Akt signaling pathway related proteins.The TUNEL assay was used to detect the apoptosis of U2OS osteosarcoma cells.The above experiments were repeated three times to ensure the accuracy of the experimental results.Results:After U2OS osteosarcoma cells were treated with Butein,the cell activity of U2OS osteosarcoma was decreased significantly.The expression of Bax proteinwas increased,while the expression of Bcl-2,MMP-2 and MMP-9 was decreased.In addition,when U2OS osteosarcoma cells were treated with Butein,the expression of PI3K-Akt signaling pathway was decreased.Conclusion:Butein promotes the apoptosis of U2OS osteosarcoma and suppresses its invasion and metastasis.The results may suggest that Butein exhibits antitumor activities by suppressing the PI3K-Akt signaling pathway.