m6A readers, writers, erasers, and the m6A epitranscriptome in breast cancer

被引:26
作者
Petri, Belinda J. [1 ]
Klinge, Carolyn M. [1 ,2 ]
机构
[1] Univ Louisville Sch Med, Dept Biochem & Mol Genet, Louisville, KY 40202 USA
[2] Univ Louisville, Ctr Integrat Environm Hlth Sci CIEHS, Louisvillle, KY 40292 USA
基金
美国国家卫生研究院;
关键词
epitranscriptome; m6A; mRNA; breast cancer; RNA-BINDING PROTEIN; HETEROGENEOUS NUCLEAR RIBONUCLEOPROTEINS; ADJUVANT ENDOCRINE THERAPY; DNA-DAMAGE REPAIR; MESSENGER-RNA; GENETIC SUSCEPTIBILITY; M6A-DEPENDENT MANNER; CELL-PROLIFERATION; AMERICAN SOCIETY; POOR-PROGNOSIS;
D O I
10.1530/JME-22-0110
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Epitranscriptomic modification of RNA regulates human development, health, and disease. The true diversity of the transcriptome in breast cancer including chemical modification of transcribed RNA (epitranscriptomics) is not well understood due to limitations of technology and bioinformatic analysis. N-6-methyladenosine (m6A) is the most abundant epitranscriptomic modification of mRNA and regulates splicing, stability, translation, and intracellular localization of transcripts depending on m6A association with reader RNA-binding proteins. m6A methylation is catalyzed by the METTL3 complex and removed by specific m6A demethylase ALKBH5, with the role of FTO as an 'eraser' uncertain. In this review, we provide an overview of epitranscriptomics related to mRNA and focus on m6A in mRNA and its detection. We summarize current knowledge on altered levels of writers, readers, and erasers of m6A and their roles in breast cancer and their association with prognosis. We summarize studies identifying m6A peaks and sites in genes in breast cancer cells.
引用
收藏
页数:26
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