硼替佐米增加HL-60细胞对TRAIL的敏感性

Effect of Bortezomib on Sensitization of HL-60 Cells to TRAIL

本研究旨在探讨硼替佐米(bortezomib)是否可以增加HL-60细胞对肿瘤坏死因子相关凋亡诱导配体(TNF-related apoptosis-inducing ligand,TRAIL)的敏感性及其可能的作用机制。选择亚细胞毒浓度的硼替佐米与不同浓度的TRAIL联合处理HL-60细胞,用MTT法检测并绘制增殖抑制曲线,用Annexin V/PI双染色流式细胞术检测细胞凋亡,Western blot检测caspase-8的表达。结果表明,亚细胞毒浓度的硼替佐米与10ng/ml的TRAIL联合作用于HL-60细胞时细胞凋亡率较单独应用TRAIL时增加,相应的caspase-8的表达也随之增加。结论:亚细胞毒浓度的硼替佐米可以增加HL-60细胞对TRAIL的敏感性,其机制可能与促进caspase-8表达有关。

This study was aimed to explore whether bortezomib can sensitize HL-60 cells to TNF-related apoptosisinducing ligand （TRAIL） and to investigate its possible mechanism. The HL-60 cells were treated by different concentrations of TRAIL combined with subtoxic concentration of bortezomib. The proliferative inhibition of treated HL-60 cell was analysed by MTT assay. The cell apoptosis was determined by flow cytometry with Annexin V/PI double staining and the expression of caspase-8 was detected by Western blot. The results showed that the subtoxic concentration of bortezomib combined with l0 ng/ml of TRAIL enhanced apoptosis of HL-60 cells, as compared with TRAIL used alone; the expression of caspase-8 increased correspondingly. It is concluded that subtoxic concentration of bortezomib can sensitize HL-60 cells to TRAIL and its mechanism may be related to upregulation of caspase-8 expression.