急性髓细胞白血病中hedgehog-Gli信号通路与阿糖胞苷耐药的研究进展

Research progress of hedgehog-Gli signal pathway and cytarabine resistance in acute myeioid leukemia

耐药与复发为当前急性髓细胞白血病（AML）治疗的瓶颈，克服AML细胞耐药为提高AML疗效、达到治愈目的的关键。阿糖胞苷（eytarabine）作为AML治疗中不可或缺的重要化疗药物，其耐药越来越受到相关研究的重视。近来，多项研究证实异常激活的hedgehog（Hh）-胶质瘤相关癌基因（Gli）信号通路在阿糖胞苷耐药中发挥重要作用，且Gli基因过表达为AML不良预后标志。Hh-Gli信号通路抑制剂，尤其是Gli特异性小分子抑制剂GANT61可抑制AML细胞生长并促进其凋亡。笔者拟就AML中Hh—Gli信号通路与阿糖胞苷耐药关系进行综述。

Drug resistance and relapse are bottlenecks of acute myeloid leukemia（AML） treatment, and conquering the drug resistance of AML cells is the key to improving treatment and helping patients fully recovered. As an indispensably crucial chemotherapeutic agent of AML treatment, drug resistance of cytarabine is getting increasing attention. Recently, several studies had demonstrated that the incorrectly triggered hedgehog （Hh）-glioma-associated oncogene （Gli） signal pathway plays a significant role in the drug resistance of cytarabine. Furthermore, Gli gene over-expression is the marker of AML poor prognosis. The inhibitor of Hh-Gli signal pathway, especially Gli specific small molecular inhibitor GANT61 is capable of inhibiting growth and accelerating apoptosis of AML ceils. Therefore, this aricle reviews literatures on the relationship between the signaling pathway of Hh-Gli and drug resistance of cytarabine in AML.