β-及γ-catenin与急性髓细胞白血病关系的研究进展

Ressearch progress of the relationships between β-,γ-catenin and acute myeloid leukemia

β-及γ-catenin均参与白血病干细胞（LSC）的自我更新过程，在急性髓细胞白血病（AML）中存在异常表达及易位，因此其可能成为清除LSC的新治疗靶点。β-catenin是经典Wnt信号通路中的关键细胞因子，其异常表达及核易位是AML预后不良的独立危险因素。新近研究结果显示，体外抑制β-catenin表达可以杀伤AML及其LSC。而γ-catenin是β-catenin的同源蛋白，在白血病中可以通过β-catenin依赖或非依赖途径发挥生物学作用。笔者就近年来，β-及γ-catenin在AML及其LSC中的研究进展进行综述。

Overexpression and aberrant nuclear localization of β-catenin and γ-catenin is frequent in acute myelogenous leukemia （AML）. They participate in the process of the leukemia stem cell （LSC） self- renewal, and may be important targets for elimination of LSC. β-catenin is a key signal transducer factor in the canonical Wnt pathway, and its abnormal expression and nuclear translocation is an independent risk factor for poor prognosis in AML. Recent studies showed that inhibition of β-catenin can kill AML and its LSC in vitro. γ-catenin, as a homologous protein to β-catenin, plays its biologic role through dependent or non-dependent on the β-catenin pathway. This article reviews literatures on advances of β-catenin and γ-eatenin in AML and its LSC.