Yoshida A, Ueda T
First Department of Internal Medicine, Fukui Medical School.
Nihon Rinsho. 1996 Jul;54(7):1822-7.
Many anticancer agents induce apoptosis in human leukemia cells. Among the various leukemia cells, especially HL-60 cells and U937 cells are very sensitive to apoptosis upon anticancer agents treatment. A serine protease inhibitor TPCK and an ICE-like protease inhibitor VAD-FMK prevented etoposide, camptothecin and ara-C-induced internucleosomal DNA cleavage in human myeloid leukemia HL-60 and U937 cells. Using a cell-free system, we have examined the inhibitory mechanism of these inhibitors on anticancer agent-induced internucleosomal DNA cleavage. Our data indicate that serine and ICE-like proteases may be involved in anticancer agent-induced apoptosis at the different stages, and especially a serine protease may be closely associated with the final step for induction of DNA fragmentation during apoptosis in human myeloid leukemia HL-60 and U937 cells.
许多抗癌药物可诱导人白血病细胞凋亡。在各种白血病细胞中，尤其是HL - 60细胞和U937细胞对抗癌药物治疗诱导的凋亡非常敏感。丝氨酸蛋白酶抑制剂TPCK和ICE样蛋白酶抑制剂VAD - FMK可阻止依托泊苷、喜树碱和阿糖胞苷诱导的人髓性白血病HL - 60和U937细胞的核小体间DNA裂解。利用无细胞系统，我们研究了这些抑制剂对抗癌药物诱导的核小体间DNA裂解的抑制机制。我们的数据表明，丝氨酸蛋白酶和ICE样蛋白酶可能在不同阶段参与抗癌药物诱导的凋亡，尤其是丝氨酸蛋白酶可能与人髓性白血病HL - 60和U937细胞凋亡过程中DNA片段化诱导的最后一步密切相关。
