IGF2BP2: an m6A reader that affects cellular function and disease progression
Insulin-like growth factor 2 messenger RNA (mRNA)-binding protein 2 (IGF2BP2) is a widely studied N 6 -methyladenosine (m 6 A) modification reader, primarily functioning to recognize and bind to m 6 A modification sites on the mRNA of downstream target genes, thereby enhancing their stability. Previ...
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Published in | Cellular & molecular biology letters Vol. 30; no. 1; pp. 43 - 32 |
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Main Authors | , , , , |
Format | Journal Article |
Language | English |
Published |
Wrocław
BioMed Central
09.04.2025
BMC |
Subjects | |
Online Access | Get full text |
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Summary: | Insulin-like growth factor 2 messenger RNA (mRNA)-binding protein 2 (IGF2BP2) is a widely studied N 6 -methyladenosine (m 6 A) modification reader, primarily functioning to recognize and bind to m 6 A modification sites on the mRNA of downstream target genes, thereby enhancing their stability. Previous studies have suggested that the IGF2BP2-m 6 A modification plays an essential role in cellular functions and the progression of various diseases. In this review, we focus on summarizing the molecular mechanisms by which IGF2BP2 enhances the mRNA stability of downstream target genes through m 6 A modification, thereby regulating cell ferroptosis, epithelial–mesenchymal transition (EMT), stemness, angiogenesis, inflammatory responses, and lipid metabolism, ultimately affecting disease progression. Additionally, we update the related research progress on IGF2BP2. This article aims to elucidate the effects of IGF2BP2 on cell ferroptosis, EMT, stemness, angiogenesis, inflammatory responses, and lipid metabolism, providing a new perspective for a comprehensive understanding of the relationship between IGF2BP2 and cell functions such as ferroptosis and EMT, as well as the potential for targeted IGF2BP2 therapy for tumors and other diseases. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 ObjectType-Review-3 content type line 23 |
ISSN: | 1689-1392 1425-8153 1689-1392 |
DOI: | 10.1186/s11658-025-00723-9 |