N6-methyladenosine reader YTHDF2 in cell state transition and antitumor immunity
- 1The Laboratory of Microbiome and Microecological Technology, Institute of Microbiology, Chinese Academy of Sciences, Beijing 100101, China
- 2Department of Radiation and Cellular Oncology, University of Chicago, Chicago, Illinois 60637, USA
- 3Ludwig Center for Metastasis Research, University of Chicago, Chicago, Illinois 60637, USA
- 4Department of Chemistry, The University of Chicago, Chicago, Illinois 60637, USA
- 5Howard Hughes Medical Institute, The University of Chicago, Chicago, Illinois 60637, USA
- 6Department of Biochemistry and Molecular Biology, Institute for Biophysical Dynamics, The University of Chicago, Chicago, Illinois 60637, USA
- Corresponding authors: wangll{at}im.ac.cn, chuanhe{at}uchicago.edu
Abstract
Recent studies have revealed that the YTHDF family proteins bind preferentially to the N6-methyladenosine (m6A)-modified mRNA and regulate the functions of these RNAs in different cell types. YTHDF2, the first identified m6A reader in mammals, has garnered significant attention because of its profound effect to regulate the m6A epitranscriptome in multiple biological processes. Here, we review current knowledge on the mechanisms by which YTHDF2 exerts its functions and discuss recent advances that underscore the multifaceted role of YTHDF2 in development, stem cell expansion, and immune evasion. We also highlight potential therapeutic interventions targeting the m6A/YTHDF2 axis to improve the response to current antitumor therapies.
This article, published in RNA, is available under a Creative Commons License (Attribution-NonCommercial 4.0 International), as described at http://creativecommons.org/licenses/by-nc/4.0/.
