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IGF2BP1—An Oncofetal RNA-Binding Protein Fuels Tumor Virus Propagation
The oncofetal RNA-binding protein IGF2BP1 has been reported to be a driver of tumor progression in a multitude of cancer entities. Its main function is the stabilization of target transcripts by shielding these from miRNA-mediated degradation. However, there is growing evidence that several virus sp...
Autores principales: | , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10385356/ https://www.ncbi.nlm.nih.gov/pubmed/37515119 http://dx.doi.org/10.3390/v15071431 |
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author | Glaß, Markus Hüttelmaier, Stefan |
author_facet | Glaß, Markus Hüttelmaier, Stefan |
author_sort | Glaß, Markus |
collection | PubMed |
description | The oncofetal RNA-binding protein IGF2BP1 has been reported to be a driver of tumor progression in a multitude of cancer entities. Its main function is the stabilization of target transcripts by shielding these from miRNA-mediated degradation. However, there is growing evidence that several virus species recruit IGF2BP1 to promote their propagation. In particular, tumor-promoting viruses, such as hepatitis B/C and human papillomaviruses, benefit from IGF2BP1. Moreover, recent evidence suggests that non-oncogenic viruses, such as SARS-CoV-2, also take advantage of IGF2BP1. The only virus inhibited by IGF2BP1 reported to date is HIV-1. This review summarizes the current knowledge about the interactions between IGF2BP1 and different virus species. It further recapitulates several findings by presenting analyses from publicly available high-throughput datasets. |
format | Online Article Text |
id | pubmed-10385356 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-103853562023-07-30 IGF2BP1—An Oncofetal RNA-Binding Protein Fuels Tumor Virus Propagation Glaß, Markus Hüttelmaier, Stefan Viruses Review The oncofetal RNA-binding protein IGF2BP1 has been reported to be a driver of tumor progression in a multitude of cancer entities. Its main function is the stabilization of target transcripts by shielding these from miRNA-mediated degradation. However, there is growing evidence that several virus species recruit IGF2BP1 to promote their propagation. In particular, tumor-promoting viruses, such as hepatitis B/C and human papillomaviruses, benefit from IGF2BP1. Moreover, recent evidence suggests that non-oncogenic viruses, such as SARS-CoV-2, also take advantage of IGF2BP1. The only virus inhibited by IGF2BP1 reported to date is HIV-1. This review summarizes the current knowledge about the interactions between IGF2BP1 and different virus species. It further recapitulates several findings by presenting analyses from publicly available high-throughput datasets. MDPI 2023-06-24 /pmc/articles/PMC10385356/ /pubmed/37515119 http://dx.doi.org/10.3390/v15071431 Text en © 2023 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Review Glaß, Markus Hüttelmaier, Stefan IGF2BP1—An Oncofetal RNA-Binding Protein Fuels Tumor Virus Propagation |
title | IGF2BP1—An Oncofetal RNA-Binding Protein Fuels Tumor Virus Propagation |
title_full | IGF2BP1—An Oncofetal RNA-Binding Protein Fuels Tumor Virus Propagation |
title_fullStr | IGF2BP1—An Oncofetal RNA-Binding Protein Fuels Tumor Virus Propagation |
title_full_unstemmed | IGF2BP1—An Oncofetal RNA-Binding Protein Fuels Tumor Virus Propagation |
title_short | IGF2BP1—An Oncofetal RNA-Binding Protein Fuels Tumor Virus Propagation |
title_sort | igf2bp1—an oncofetal rna-binding protein fuels tumor virus propagation |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10385356/ https://www.ncbi.nlm.nih.gov/pubmed/37515119 http://dx.doi.org/10.3390/v15071431 |
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