YT521-B homology domain family proteins as N6-methyladenosine readers in tumors

Heng Yang; Chengyao Chiang; Qinhong Luo; Chunlan Chen; Junrong Huang; Lizhi Zhu; Duo Zheng

doi:10.3389/fgene.2022.934223

YT521-B homology domain family proteins as N6-methyladenosine readers in tumors

Front Genet. 2022 Aug 9:13:934223. doi: 10.3389/fgene.2022.934223. eCollection 2022.

Authors

Heng Yang¹, Chengyao Chiang^{1

2}, Qinhong Luo¹, Chunlan Chen¹, Junrong Huang¹, Lizhi Zhu¹, Duo Zheng¹

Affiliations

¹ Guangdong Provincial Key Laboratory of Genome Stability and Disease Prevention, Shenzhen University International Cancer Center, Department of Cell Biology and Genetics, School of Medicine, Department of Pharmacy, The First Affiliated Hospital of Shenzhen University, Shenzhen Second People's Hospital (Shenzhen Institute of Translational Medicine), Guangdong Key Laboratory for Biomedical Measurements and Ultrasound Imaging, Shenzhen University, Shenzhen, China.
² Central Laboratory, Southern University of Science and Technology, Yantain Hospital, Shenzhen, China.

Abstract

N6-methyladenosine (m6A) is the most abundant internal chemical modification of eukaryotic mRNA and plays diverse roles in gene regulation. The m6A modification plays a significant role in numerous cancer types, including kidney, stomach, lung, bladder tumors, and melanoma, through varied mechanisms. As direct m6A readers, the YT521-B homology domain family proteins (YTHDFs) play a key role in tumor transcription, translation, protein synthesis, tumor stemness, epithelial-mesenchymal transition (EMT), immune escape, and chemotherapy resistance. An in-depth understanding of the molecular mechanism of YTHDFs is expected to provide new strategies for tumor treatment. In this review, we provide a systematic description of YTHDF protein structure and its function in tumor progression.

Keywords: EMT; M6A; YTHDFs; chemotherapy resistance; immune escape; tumor.

Publication types

Review