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通过FTO的内基序列调节的急性髓性白血病的分化阻断

Francesco Camera¹, Isabel Romero-Camarero¹, Bradley H Revell¹

¹Leukaemia Biology Laboratory, Cancer Research UK Manchester Institute, The University of Manchester, The Oglesby Cancer Research Centre Building, 555 Wilmslow Road, M20 4GJ Manchester, UK.

|August 4, 2023

概括

在FTO内8中的一个调节模块阻碍了急性髓性白血病 (AML) 中的髓状细胞分化. 这种FTO长非编码RNA (lncRNA) 影响IRX3表达和AML细胞分化.

科学领域:

遗传学遗传学是一个
分子生物学分子生物学
癌症研究癌症研究

背景情况:

* 伊洛quois转录因子基因IRX3在急性髓性白血病 (AML) 中高度表达,导致分化阻断.
*位于IRX3的下游约220kB的FTO内8序列显示了监管潜力.

研究的目的:

* 调查FTO内部8元素在IRX3表达和AML病变发生中的调控作用.
* 为了确定FTO-lncAML活动在AML细胞中的功能后果.

主要方法:

*在FTO内8中分析了基因组乙化和DNA甲基化.
* 染色体形状捕获以评估FTO内8:IRX3促进体接触.
*使用RNAseq.对FTO-lncAML和IRX3进行敲除 (KD).
*对AML细胞分化和克隆原性活动的评估.

主要成果:

*删除FTO内部8元素证实了它们在IRX3.3上的积极监管作用.
* FTO 内子8 携带长非编码RNA (lncRNA) 转录 (FTO-lncAML).
* FTO-lncAML KD诱导了AML细胞分化,降低了克隆原性,并降低了FTO内核8:IRX3促进体接触.
* FTO-lncAML KD,但不是IRX3 KD,降低调节的HOXA,表明转作用活性.
* FTO-lncAML高AML样本显示HOXA高,基因表达差异较低.

结论:

* 在FTO内8个内部的一个调节模块,包括增强元件和一个lncRNA,在人类AML中是活跃的.
* 该模块积极调节IRX3并阻碍骨髓分化.
* FTO-lncAML通过影响HOXA表达和分化途径,在维持AML表型方面发挥着关键作用.

关键词:

癌症癌症癌症癌症表观遗传学在表观遗传学中,表观遗传学是指表观遗传学.基因调节的分子机制文字转录学 (Transcriptomics) 是一个学科.

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