Caspases在TRAIL诱导MG-63骨肉瘤细胞株凋亡中的作用

目的 :初步观察并探讨人重组可溶性肿瘤坏死因子相关凋亡诱导配体 (TNF relatedapoptosis inducinglig and ,TRAIL)蛋白诱导MG 6 3骨肉瘤细胞凋亡的作用机制。方法 :用RT PCR检测TRAIL受体在MG 6 3骨肉瘤细胞上的表达 ;用MTT试验检测TRAIL对MG 6 3细胞的抑制率及加入Caspase抑制剂后TRAIL对MG 6 3骨肉瘤细胞株抑制率的变化。初步分析TRAIL诱导MG 6 3骨肉瘤细胞株凋亡的作用机理。结果 :当TRAIL单独作用于MG 6 3骨肉瘤细胞株时 ,可产生明显的抑制效果 ;而当TRAIL分别加入广谱的Caspase抑制剂zVAD FMK、Caspase 8的抑制剂zIETD FMK、Caspase 3的抑制剂zDEVD FMK与细胞株MG 6 3共同孵育时 ,TRAIL的抑制作用均被阻断。结论 :TRAIL可能是通过与细胞膜表面的死亡受体结合 ,然后激发细胞内Caspase级联反应从而诱导肿瘤细胞凋亡的。

Role of Caspases during TNF-related Apoptosis-inducing Ligand Killing Osteosrarcoma Cell Lines

Objective: To investigate molecular mechanism of TNF-related apoptosis-inducing ligand(TRAIL)-induced apoptosis in MG-63 osteosarcoma cell line. Methods: To assess rTRAIL-mediated cytotoxicity in MG-63 osteosarcoma cell line, MG-63 cells were treated for 24 hours with different concentration of sTRAIL and cell death was evaluated with the MTT assay.To evaluate effect of Caspase inhibitors, MG-63 cell line was treated with sTRAIL and zVAD-FMK, zIETD-FMK or zDEVD-FMK respectively. The expression of TRAIL receptors in MG-63 osteosarcoma cell line was studied with RT-PCR. Results: MG-63 osteosarcoma cell line was sensitive to sTRAIL, but it was resistant to apoptosis when treated with sTRAIL and Caspase inhibitors. Conclusion: TRAIL could establish a complex with death receptors and activate Caspase casade, which induced apoptosis in MG-63 osteosarcoma cell line.