scispace - formally typeset
Open AccessJournal ArticleDOI

The role of Insulin-like growth factor 2 mRNA-binding proteins (IGF2BPs) as m6A readers in cancer

TLDR
The up-to-date knowledges of IGF2BPs (IGF2BP1/2/3) as m6A readers in an m6a-modified manner in cancer progression are reviewed, and the oncogenic role of IGF 2BPs in cancer is discussed.
Abstract
RNA can be modified by over 170 types of distinct chemical modifications, and the most abundant internal modification of mRNA in eukaryotes is N6-methyladenosine (m6A). The m6A modification accelerates mRNA process, including mRNA splicing, translation, transcript stability, export and decay. m6A RNA modification is installed by methyltransferase-like proteins (writers), and potentially removed by demethylases (erasers), and this process is recognized by m6A-binding proteins (readers). Notably, alterations of m6A-modified proteins (writers, erasers and readers) are involved in the tumorigenesis, progression and metastasis. Importantly, the fate of m6A-methylated mRNA is mediated mostly through m6A readers, and among these readers, insulin-like growth factor 2 mRNA-binding proteins (IGF2BPs) are unique RNA-binding proteins (RBPs) that stabilize their targets mRNA via m6A modification. In this review, we update the writers, erasers and readers, and their cross-talks in m6A modification, and briefly discuss the oncogenic role of IGF2BPs in cancer. Most importantly, we mainly review the up-to-date knowledges of IGF2BPs (IGF2BP1/2/3) as m6A readers in an m6A-modified manner in cancer progression.

read more

Content maybe subject to copyright    Report

Citations
More filters
Journal ArticleDOI

RNA modifications: importance in immune cell biology and related diseases

TL;DR: In this article , the authors present existing knowledge of the biological functions and underlying mechanisms of RNA modifications, including N 6 -methyladenosine (m 6 A), 5-methylcytosine(m 5 C), N 1 -methyl adenosine,m 1 A), N 7 -methylguanosine (n 7 G), N 4 -acetylacetylcytusine (ac 4 C), pseudouridine (Ψ), uridylation, and A-to-I RNA editing, and summarize their critical roles in immune cell biology and highlight the challenges and future directions based on the existing knowledge.
Journal ArticleDOI

FTO Inhibits Epithelial Ovarian Cancer Progression by Destabilising SNAI1 mRNA through IGF2BP2

TL;DR: It is found that FTO was downregulated with increased m6A levels in EOC and the FTO-IGF2BP2-SNAI1 axis is a potential therapeutic target in E OC.
Journal ArticleDOI

Stabilization of IGF2BP1 by USP10 promotes breast cancer metastasis via CPT1A in an m6A-dependent manner

TL;DR: Wang et al. as discussed by the authors showed that USP10 can bind to, deubiquitinate, and stabilize IGF2BP1, resulting in its higher expression level in breast cancer.
Journal ArticleDOI

Inhibition of IGF2BP1 attenuates renal injury and inflammation by alleviating m6A modifications and E2F1/MIF pathway

TL;DR: A putative m6A recognition site was identified at the 3′-UTR region of E2F transcription factor 1 (E2F1) mRNA via bioinformatics analyses and validated using mutation and luciferase experiments as mentioned in this paper .
Journal ArticleDOI

RNA m6A methylation regulators in endometrial cancer (Review)

TL;DR: In this paper , the current status of research on m6A methylation in endometrial cancer was reviewed and the mechanisms of methyltransferase, demethylase and m6a binding protein in regulating the development and progression of EC by modifying mRNA were introduced.
References
More filters
Journal ArticleDOI

Comprehensive Analysis of mRNA Methylation Reveals Enrichment in 3′ UTRs and near Stop Codons

TL;DR: A method is presented for transcriptome-wide m(6)A localization, which combines m( 6)A-specific methylated RNA immunoprecipitation with next-generation sequencing (MeRIP-Seq) and reveals insights into the epigenetic regulation of the mammalian transcriptome.
Journal ArticleDOI

N6-methyladenosine-dependent regulation of messenger RNA stability

TL;DR: It is shown that m6A is selectively recognized by the human YTH domain family 2 (YTHDF2) ‘reader’ protein to regulate mRNA degradation and established the role of YTH DF2 in RNA metabolism, showing that binding of Y THDF2 results in the localization of bound mRNA from the translatable pool to mRNA decay sites, such as processing bodies.
Journal ArticleDOI

N6-methyladenosine in nuclear RNA is a major substrate of the obesity-associated FTO.

TL;DR: FTO exhibits efficient oxidative demethylation activity of abundant N6-methyladenosine (m6A) residues in RNA in vitro, and it is shown that FTO partially colocalizes with nuclear speckles, supporting m6A in nuclear RNA as a physiological substrate of FTO.
Related Papers (5)