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Cancer Cell:重审FTO在白血病中的癌基因作用

2017-05-15 黄蔚 BioArt

5月8日,Cancer cell在线发表来自德克萨斯大学健康科学中心Ricardo C.T.Aguiar课题组题为“IDH Mutation, Competitive Inhibition of FTO, and RNA Methylation”的Letter类型文章(下图)。

5月8日,Cancer cell在线发表来自德克萨斯大学健康科学中心Ricardo C.T.Aguiar课题组题为“IDH Mutation, Competitive Inhibition of FTO, and RNA Methylation”的Letter类型文章(下图)。该研究将矛头直指芝加哥大学陈建军老师与何川老师此前合作的文章“FTO Plays an Oncogenic Role in Acute Myeloid Leukemia as a N6-Methyladenosine RNA Demethylase”(详见BioArt此前的报道:芝大陈建军、何川组Cancer Cell报道肥胖基因FTO过表达导致白血病丨BioArt聚焦),认为在研究FTO在急性髓系白血病(AML)中作为癌基因的作用时,应考虑占AML约20%的IDH突变,因为IDH-mutation可以竞争性地抑制FTO的活性,在不影响FTO表达量的情况下 ,提高m6A的整体水平。



FTO是α-酮戊二酸(α-KG)依赖的双加氧酶,可去除RNA上的m6A修饰。陈建军组通过临床芯片数据分析,发现FTO在含PML-RARA,MLL融合基因以及FLT3-ITD/NPM1-mut的AML亚型中表达升高,并通过体内和体外实验证明FTO通过其去甲基化酶的功能,调节RNA m6A水平,促进PML-RARA和MLL融合基因型白血病的发展。

有趣的是,突变的IDH1/2正好可以将α-KG还原为D2-HG,使α-KG的水平降低,导致α-KG依赖的双加氧酶无法发挥酶活性。IDH-mut可以抑制依赖α-KG的DNA羟化酶(TET家族蛋白)和组蛋白去甲基化酶(Jumonji家族)的活性,所以高甲基化水平正是IDH-mutant AML的特征。

那么关键问题来了,突变的IDH是否可以抑制也是α-KG 依赖的FTO的活性呢?

在这篇Letter论文中,研究人员首先检测了突变的IDH是否能影响m6A的整体水平。通过在293T细胞中稳定过表达野生型IDH以及2种IDH突变体——IDH2 R140Q和IDH2 R172K,发现过表达突变型IDH可以显着的升高RNA m6A水平(下图)。



同时,细胞接受突变型IDH抑制剂AG-221处理后,FTO的表达不受影响,而IDH-mut细胞的m6A水平降低(下图)。



以上结果说明IDH-mut可以显着地提高m6A水平,那么FTO在IDH-mut的细胞中是否仍发挥去甲基化酶的作用呢?研究者利用CRISPR构建了FTO敲除(FTO KO)的细胞系,并假设,如果IDH-mut是通过竞争性的抑制FTO活性来实现m6A的增加,那么敲除FTO将对IDH-mut细胞的m6A水平没有影响,却能提高野生型IDH细胞的m6A水平。正如他们假设的一样,m6A在IDH2-WT/FTO-KO细胞中显着上升,而在IDH2-MUT/FTO-KO细胞中几乎没有变化(下图)。



接下来研究者回归AML体系,检测了一系列AML原代细胞的m6A水平,发现即使这些细胞的FTO及ALKBH5的表达水平相当,但IDH1/2-mutant细胞的m6A显着高于IDH1/2-WT细胞(下图)。



有趣的是,与陈建军老师的结果一致, 5个高表达FTO的细胞均携带FLT3-ITD/NPM1-mut,其中2个还是IDH1/2 mutations。考虑到FLT3-ITD/NPM1-mut与IDH1/2 mutations存在联系,可见FTO的表达调控非常复杂,并且其表达量与活性强度的关系还有待考证。研究者认为在IDH1/2 mutations的AML中,很难验证FTO表达量与m6A水平以及靶基因表达之间的关系,因为IDH1/2 mutations不仅影响了RNA m6A修饰,也调控了DNA甲基化和组蛋白甲基化水平,将基因的变化简单的归结为某一种表观遗传修饰是不恰当的。

认为这是一篇火药味极重,想要反驳FTO在AML中作用的小伙伴们,看到这里可以松一口气了。该研究并没有涉及陈建军组研究中的主要细胞模型——含PML-RARA和MLL融合基因的细胞,而主要是对IDH-MUT型AML中FTO及m6A的作用提出了新的理论。值得注意的是,ALKBH5也是α-KG依赖的RNA m6A去甲基化酶,Cancer Cell另一篇有关RNA m6A的文章“m6A Demethylase ALKBH5 Maintains Tumorigenicity of Glioblastoma Stem-like Cells by Sustaining FOXM1 Expression and Cell Proliferation Program”(详见BioArt此前的报道:连续两篇论文揭示RNA m6A修饰在恶性胶质瘤中作用丨BioArt特别推荐),在恶性胶质瘤中研究了ALKBH5作为癌基因的功能,而IDH突变在恶性胶质瘤中也有发生,是一种预后佳的突变。此二者之间是否有联系尚待研究。

Ricardo C.T.Aguiar的研究是对RNA m6A在肿瘤中作用的补充和开拓,稍有遗憾的是,该研究未进一步探究m6A在IDH-mut型AML中的升高导致的基因变化以及是否是IDH-mut致病的关键。IDH-mut将RNA与DNA,组蛋白修饰联系到一起,可见细胞中的表观遗传是交错复杂的,未来也期待更多的研究为我们揭开其中的奥秘。

原始出处:

Elkashef SM, Lin AP, Myers J,et al.IDH Mutation, Competitive Inhibition of FTO, and RNA Methylation.Cancer Cell.

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    2017-10-16 维他命
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    2017-05-18 飘飘爱

    很好

    0

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    2017-05-17 仁者大医
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    2017-05-15 蔬菜

    写的非常精彩

    0

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    2017-05-15 三生有幸9135

    学习一下谢谢分享

    0

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