Ren H, Chen S, Lu D
Institute of Hematology, People's Hospital, Beijing Medical University, Beijing 100044, China.
Chin Med J (Engl). 1998 Aug;111(8):678-81.
To explore the anti-apoptotic mechanism and the effective apoptosis-inducing method in chronic myelogenous leukemia (CML) cells.
K562 cell line was used to observe the effect of combination of herbimycin A (HMA), a tyrosine kinase inhibitor, and chemotherapeutic agents on the induction of apoptosis.
HMA or chemotherapeutic agents could inhibit the proliferation but not significantly induce apoptosis of K562 cells. However, HMA significantly enhanced apoptosis when combined with chemotherapeutic agents. Addition of sulfhydryl compound to the cultures to conjugate HMA completely abrogated this enhancing effect on K562 cells.
HMA increases the sensitivity of CML cells to chemotherapeutic agents by inactivating tyrosine kinase activity. It is promising that combination of HMA with conventional chemotherapeutic drugs may be a new strategy in the treatment of CML.
探讨慢性粒细胞白血病（CML）细胞的抗凋亡机制及有效的凋亡诱导方法。
利用K562细胞系观察酪氨酸激酶抑制剂赫曲霉素A（HMA）与化疗药物联合应用对凋亡诱导的影响。
HMA或化疗药物可抑制K562细胞增殖，但不能显著诱导其凋亡。然而，HMA与化疗药物联合应用时可显著增强凋亡。向培养物中添加巯基化合物以结合HMA可完全消除对K562细胞的这种增强作用。
HMA通过使酪氨酸激酶活性失活增加CML细胞对化疗药物的敏感性。HMA与传统化疗药物联合应用有望成为治疗CML的新策略。
