AML1-ETO inhibits acute myeloid leukemia immune escape by CD48

Abstract

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.

Keywords:

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

Acknowledgements

The authors thank LetPub (www.letpub.com) for providing linguistic assistance during the preparation of this manuscript.

Disclosure statement

No potential conflict of interest was reported by the author(s).

Data availability statement

We declared that the materials described in the manuscript, including all the relevant raw data, are freely available to any scientist wishing to use these for noncommercial purposes, without breaching participant confidentiality.

Additional information

Funding

The Key Program of National Natural Science Foundation of China [Grant number 82030076], National Natural Science Foundation of China [Grant numbers 81670162 and 81470010], National Science and Technology Major Project of China [Grant number 2019ZX09201-002-003] supported this study.