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乙型肝炎病毒介导的m6A脱甲基化增加肝细胞癌干细胞和免疫逃生

Yuting Meng¹, Zheyue Shu², Xueyao Wang³

¹State Key Laboratory for Diagnosis and Treatment of Infectious Diseases, National Clinical Research Center for Infectious Diseases, National Medical Center for Infectious Diseases, Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, P.R. China.

Molecular cancer research : MCR

|March 28, 2024

概括

乙型肝炎病毒 (HBV) 感染通过稳定ALKBH5mRNA降低了肝癌中的N6-甲基氨酸 (m6A) 水平. 这通过ALKBH5/SNAI2通路促进癌症干和免疫逃避.

科学领域:

肝细胞癌研究肝细胞癌研究
表观遗传学在表观遗传学中,表观遗传学是指表观遗传学.
病毒瘤学病毒瘤学

背景情况:

持续性乙型肝炎病毒 (HBV) 感染是肝细胞癌 (HCC) 的关键驱动因素.
N6-甲基氨酸 (m6A) 修饰与各种癌症有关,但它们在与HBV相关的HCC干系中的作用尚不清楚.

研究的目的:

阐明m6A修饰在HBV阳性HCC中维持干性的调节机制.
调查ALKBH5及其下游标在HBV相关肝癌进展中的作用.

主要方法:

在HBV阳性HCC中分析m6A修饰水平.
研究ALKBH5mRNA的稳定性.
功能性试验评估ALKBH5在干性和自我更新中的作用.
在ALKBH5/SNAI2/YTHDF2轴上的机制研究.
评估免疫检查点连接体CD155的表达.

主要成果:

通过增加ALKBH5mRNA稳定性,HBV通过降低HCC中的m6A修饰的调节.
在HBV阳性HCC中,ALKBH5对维持茎状性至关重要.
ALKBH5通过去甲基化m6A稳定SNAI2转录,促进癌症干细胞的特征.
ALKBH5 / SNAI2轴通过激活CD155.5来增强瘤免疫逃避.

结论:

ALKBH5通过诱导SNAI2.2的m6A脱甲基化,起到与HBV相关的HCC的关键调节者的作用.
ALKBH5/SNAI2/YTHDF2轴在HBV感染期间促进干细胞类表型和免疫逃生.

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