硼替佐米对伊马替尼耐药细胞株K562/G01增殖抑制和诱导凋亡作用的研究

 目的　探讨蛋白酶体抑制剂硼替佐米（BOR）对慢性粒细胞白血病（CML）伊马替尼耐药细胞株K562／G01的增殖抑制和诱导凋亡作用。方法　采用MTT法观察细胞的生长抑制效应；流式细胞术（FCM）检测细胞周期与凋亡。结果　K562／G01细胞对伊马替尼不敏感，伊马替尼对K562／G01和K562细胞的IC50分别是（20.09±1.38）、（0.54±0.13）μmol／L；BOR对K562／G01细胞具有增殖抑制作用，并于48 h时作用效果达高峰，IC50（23.10±2.71）nmol／L，随着BOR浓度和作用时间的增加，FCM检测可见G2／M 期细胞周期阻滞及明显的凋亡峰。结论　BOR对CML伊马替尼耐药细胞株具有增殖抑制和诱导凋亡的作用，其机制可能与细胞周期G2／M 期的阻滞有关。

Growth inhibition and apoptosis induction to imatinib-resistant cell line K562/G01 by Bortezomib

Objective To explore the effect of proteasome inhibitor bortezomib (BOR) on proliferation inhibition and apoptosis in imatinib-resistant chronic myeloid leukemia cell line K562/G01. Methods MTT assay was used to observe the effect of growth inhibitory of cells; flow cytometry was used to detect cell cycle and apoptosis. Results K562/G01 cells was not sensitive to imatinib,1C50 values of imatinib to K562 and K562/G01 cells was (20.09±1.38) and (0.54±0.13) μmol/L,respectively; BOR could inhibit proliferation in K562/G01 cell,peaked at 48 h,and IC50 value of BOR to K562/G01 was (23.10±2.71) nmol/L. G2/M phase cell cycle arrest and significant apoptosis peak could be seen by flow cytometry with increased in the concentration and action time of BOR. Conclusion BOR can inhibit proliferation and induce apoptosis in imatinib-resistant K562/G01 cell,the mechanism may be related to cell cycle G2/M phase arrest.