AML1-ETO inhibits acute myeloid leukemia immune escape by CD48

被引：14

作者：

Wang, Zhiding ^{[1
,2
]}

Guan, Wei ^{[2
]}

Wang, Mengzhen ^{[2
]}

Chen, Jinghong ^{[1
]}

Zhang, Linlin ^{[2
]}

Xiao, Yang ^{[2
]}

Wang, Lixin ^{[1
]}

Li, Yonghui ^{[1
]}

Yu, Li ^{[1
,2
]}

机构：

[1] Shenzhen Univ, Gen Hosp, Dept Hematol Oncol, Int Canc Ctr,Hlth Sci Ctr, Shenzhen, Peoples R China

[2] Chinese Peoples Liberat Army Gen Hosp, Dept Hematol, Beijing, Peoples R China

来源：

LEUKEMIA & LYMPHOMA | 2021年 / 62卷 / 04期

基金：

中国国家自然科学基金;

关键词：

AML1-ETO; AML; CD48; acetylation; NK;

D O I：

10.1080/10428194.2020.1849680

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

The t(8;21)(q22;q22) translocation is the most common chromosomal translocation in acute myeloid leukemia (AML), and it gives rise to acute myeloid gene 1 (AML1)-myeloid transforming gene 8 (ETO)-positive AML, which has a relatively favorable prognosis. CD48 is a favorable prognosis factor that is downregulated in AML patients. AML can escape immunosurveillance of natural killer (NK) cells by decreasing CD48 expression. The correlation between AML1-ETO and CD48-mediated immune evasion is not well understood. Here, we show that AML1-ETO can increase CD48 expression, which is regulated by AML1-ETO/P300-mediated acetylation. AML1-ETO can inhibit AML immune escape from NK cell recognition and killing by increasing CD48 expression. This study describes a novel mechanism by which AML1-ETO can inhibit AML immune escape by increasing CD48 acetylation, thereby providing new evidence about AML patients with AML1-ETO oncogene infusion having better clinical outcomes.

引用

页码：937 / 943

页数：7

共 23 条

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