The IGF2BP family of RNA binding proteins links epitranscriptomics to cancer

RNA binding proteins that act at the post-transcriptional level display a richness of mechanisms to modulate the transcriptional output and respond to changing cellular conditions. The family of IGF2BP proteins recognize mRNAs modified by methylation and lengthen their lifecycle in the context of st...

Full description

Saved in:
Bibliographic Details
Published in:Seminars in cancer biology 2022-11, Vol.86 (Pt 3), p.18-31
Main Authors: Ramesh-Kumar, Deepthi, Guil, Sonia
Format: Article
Language:English
Subjects:
Adenosine - chemistry
Adenosine - genetics
Adenosine - metabolism
Cancer
Epitranscriptomics
Humans
IGF2BP proteins
M6A-RNA
Methylation
Neoplasms - genetics
Neoplasms - metabolism
Noncoding RNA
RNA, Messenger - genetics
RNA, Messenger - metabolism
RNA-Binding Proteins - genetics
RNA-Binding Proteins - metabolism
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:RNA binding proteins that act at the post-transcriptional level display a richness of mechanisms to modulate the transcriptional output and respond to changing cellular conditions. The family of IGF2BP proteins recognize mRNAs modified by methylation and lengthen their lifecycle in the context of stable ribonucleoprotein particles to promote cancer progression. They are emerging as key ‘reader’ proteins in the epitranscriptomic field, driving the fate of bound substrates under physiological and disease conditions. Recent developments in the field include the recognition that noncoding substrates play crucial roles in mediating the pro-growth features of IGF2BP family, not only as regulated targets, but also as modulators of IGF2BP function themselves. In this review, we summarize the regulatory roles of IGF2BP proteins and link their molecular role as m6A modification readers to the cellular phenotype, thus providing a comprehensive insight into IGF2BP function.
ISSN:1044-579X
1096-3650
DOI:10.1016/j.semcancer.2022.05.009