Hu Rong, Zhang Rong, Li Ying-Chun, Yao Kun, Yang Ying, Hou Si-Yuan, Yang Wei, Liu Zhuo-Gang
Department of Hematology, Shengjing Hospital, China Medical University, Shenyang 110021, Liaoning Province, China.
Zhongguo Shi Yan Xue Ye Xue Za Zhi. 2010 Jun;18(3):617-20.
This study was aimed to explore whether bortezomib can sensitize HL-60 cells to TNF-related apoptosis-inducing 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 10 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.
本研究旨在探讨硼替佐米是否能使HL-60细胞对肿瘤坏死因子相关凋亡诱导配体(TRAIL)敏感,并研究其可能的机制。用不同浓度的TRAIL联合亚毒性浓度的硼替佐米处理HL-60细胞。采用MTT法分析处理后HL-60细胞的增殖抑制情况。通过Annexin V/PI双染流式细胞术测定细胞凋亡,并通过蛋白质免疫印迹法检测caspase-8的表达。结果显示,与单独使用TRAIL相比,亚毒性浓度的硼替佐米联合10 ng/ml的TRAIL可增强HL-60细胞的凋亡;caspase-8的表达相应增加。结论是亚毒性浓度的硼替佐米可使HL-60细胞对TRAIL敏感,其机制可能与caspase-8表达上调有关。