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Blood:IKAROS和CK2调控高危型B-ALL的BCL-XL表达和化疗敏感性

2020-06-03 QQY MedSci原创

CK2和IKAROS通过抑制BCL2L1(BCL-XL)表达调节对多柔比星的耐药; CK2抑制剂与多柔比星联合治疗对高危型B-ALL有协同治疗作用。

高危型B细胞急性淋巴细胞白血病(B-ALL)是一种侵袭性疾病,具有化疗耐药性的特点。高危型B-ALL的一个常见特征是肿瘤抑制因子IKAROS(由IKZF1基因编码)的功能丧失。

在本研究中,Song等发现IKAROS调节BCL2L1基因(编码bcl-xl蛋白)在人B-ALL中的表达。

功能获得性和功能丧失性实验表明,IKAROS与BCL2L1启动子结合,招募组蛋白去乙酰化酶HDAC1,并通过染色质重塑抑制BCL2L1的表达。在白血病中,致癌酪蛋白激酶II(CK2)在B-ALL中高表达,使IKAROS功能受损。CK2磷酸化后减少了BCL2L1启动子上结合的IKAROS和募集的HDAC1。这导致IKAROS介导的对BCL2L1表达抑制的丧失和BCL-XL表达增加。

BCL-XL和/或CK2表达增加以及IKAROS表达降低,均与多柔比星治疗耐药有关。用特异性抑制剂CX-4945抑制CK2可增加IKAROS与BCL2L1启动子的结合,增强IKAROS介导的BCL2L1在B-ALL中的抑制作用。CX-4945治疗增强了B-ALL对多柔比星的敏感性,并逆转了B-ALL对多柔比星的耐药性。CX-4945和多柔比星联合治疗在体外和高危型B-ALL的临床前模型中均显示出协同治疗效果。

综上所述,本研究结果揭示了一个新的信号网络,该网络参与调节白血病的化疗耐药性。本研究数据为CK2抑制剂CX-4945联合多柔比星治疗血液系统恶性肿瘤的靶向疗法的临床测试奠定了基础。

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    2020-11-29 xuqianhua
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    2020-06-05 膀胱癌
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    2020-06-05 lsndxfj
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