Leukemia：科学家发现WT1-MEG3信号通路有望成为治疗AML的新靶点

2017-12-22 MedSci MedSci原创

WT1-MEG3轴能抑制肿瘤生长，有望成为有效的治疗AML的一系列潜在的靶点。

急性髓系白血病是一种常见的成人恶性髓系细胞疾病，其产生的造血前体细胞克隆极具异质性，这些造血前体细胞表现出不同的生物学表型以及疾病进展特征，这也造成了标准化治疗效果的不确定性。为了改善AML的治疗方法，提高疾病的治愈率，目前基础与临床研究集中寻找AML的基因特征，以希望更深一步的理解AML的发病机制，从而寻找新的治疗靶点以期提高疾病的治愈率。

长非编码RNAs（Long non-coding RNAs， IncRNAs）在肿瘤发生过程中发挥着重要的作用，以最近的发现的髓系相关的IncRNA MEG3为例，它能够通过提高肿瘤抑制因子p53蛋白水平并且能够促进p53结合与它的下游靶基因，从而抑制肿瘤的生长。然而TP53突变能够导致野生型具有肿瘤抑制功能的p53丢失，而这种突变存在于多种肿瘤细胞内，包括AML。也有研究表明MEG3与RB信号通路调控有关而具有调节细胞增殖的能力，这就表明MEG3有可能参与非p53依赖的抑癌信号通路。

转录因子WT1能够在转录水平激活MEG3，WT1在AML发生中通常会因表观遗传修饰沉默或基因突变而功能失调。MEG3被认为是WT1分子的新的下游靶位点。TET2能通过将5-甲基胞嘧啶转换为5-羟甲基胞嘧啶而是DNA序列去甲基化。AML细胞中通常能够发现TET2基因突变，并且TET2突变也能够促进AML的疾病进展。研究发现WT1与TET2能互相结合，并且WT1可以募集TET2到WT1的靶基因上，这就表明TET2能够参与AML疾病中WT1的转录活性。

这个研究发现，MGE3失活能够通过p53依赖和非依赖途径促进AML白血病发生。进一步的分析表明WT1能够特异性的结合于MEG3的启动子激活转录，而TET2和WT1在AML发病过程中具有相关性。总之，TET2可以作为WT1的共同作用因子促进MEG3的转录。由于WT1-MEG3轴能抑制肿瘤生长，这个研究为有效的治疗AML提供了一系列潜在的靶点。

原文出处：Lyu Y，Lou J， Yang Y et al.Dysfunction of the WT1-MEG3 signaling promotes AML leukemogenesis via p53-dependent and -independent pathways.Leukemia. 2017 Dec；31(12)：2543-2551. doi： 10.1038/leu.2017.116. Epub 2017 Apr 12.

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2023-09-24 侠胆医心来自上海

科学家发现WT1-#MEG3#信号通路有望成为治疗#AML#的新靶点，#急性髓系白血病#

96 0
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2018-07-01 闆锋旦

#WT1#

83 0
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2018-06-05 旅苦化文_208

#科学家发现#

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2018-01-04 1209e435m98(暂无昵称)

学习了.谢谢分享

101 0
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2017-12-24 lsndxfj

#新靶点#

126 0
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2017-12-24 智者为医08

#信号通路#

85 0

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