肿瘤坏死因子相关凋亡诱导配体联合阿霉素治疗骨肉瘤

Treatment of osteosarcoma with a combination of TRAIL and doxorubicin

目的探讨肿瘤坏死因子相关凋亡诱导配体(TRAIL)与阿霉素(ADM)联用对骨肉瘤细胞株HOS是否具有协同杀伤作用,并对其机制进行初步研究。方法MTT法检测细胞的抑制率和存活率,流式细胞术(FCM)检测细胞凋亡率,逆转录-聚合酶链反应(RT-PCR)检测TRAIL受体(receptor,R)的表达水平。结果单用0.5mg/L TRAIL及1.0、10.0、100.0mg/L ADM对HOS-8603的抑制率分别为13.18%、5.56%、23.02%和76.72%,联合用药的抑制率分别为42.98%、53.12%、81.91%。0.5mg/L TRAIL和1.0mg/LADM有协同作用,TRAIL和ADM联用时TRAIL R2mRNA表达较TRAIL单用时明显增强。结论TRAIL与ADM联用对骨肉瘤细胞有明显的协同作用,其机制可能与ADM上调TRAIL R2的表达有关。

Objective To explore the role of tumor necrosis factor-related apoptosis inducing ligand （TRAIL） and the curative effectiveness of TRAIL combined with doxorublcin （ADM） in the treatment of osteosarcoma. Methods Cytotoxiclty was examined by MTT assay. Cell apoptosis was detected by flow cytometry. The expression of TRAIL receptors was measured by RT-PCR. Results The inhibitory rate of HOS-8603 cells treated with 0.5 mg/L TRAIL, 1.0, 10.0 and 100.0 mg/L ADM alone were 13.18 %, 5.56 %, 23.02 % and 76.72 % respectively. The inhibitory rate of cells treated with 0.5 mg/L TRAIL combined with 1.0,10.0 or 100.0 mg/L ADM was 42.98 %, 53.12 %, 81.91% respectively. 0.5 mg/L TRAIL and 1 mg/L ADM had synergistic cytotoxin effects in combination treatment. Conclusion TRAIL in combination with subtoxic doxorubicincuuld jointly kill HOS-8603 cells, which might be contributed to the up-regulation of TRAIL R2 expression.