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On the Role of Glycolysis in Early Tumorigenesis—Permissive and Executioner Effects
Reprogramming energy production from mitochondrial respiration to glycolysis is now considered a hallmark of cancer. When tumors grow beyond a certain size they give rise to changes in their microenvironment (e.g., hypoxia, mechanical stress) that are conducive to the upregulation of glycolysis. Ove...
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/PMC10137279/ https://www.ncbi.nlm.nih.gov/pubmed/37190033 http://dx.doi.org/10.3390/cells12081124 |
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author | Marcucci, Fabrizio Rumio, Cristiano |
author_facet | Marcucci, Fabrizio Rumio, Cristiano |
author_sort | Marcucci, Fabrizio |
collection | PubMed |
description | Reprogramming energy production from mitochondrial respiration to glycolysis is now considered a hallmark of cancer. When tumors grow beyond a certain size they give rise to changes in their microenvironment (e.g., hypoxia, mechanical stress) that are conducive to the upregulation of glycolysis. Over the years, however, it has become clear that glycolysis can also associate with the earliest steps of tumorigenesis. Thus, many of the oncoproteins most commonly involved in tumor initiation and progression upregulate glycolysis. Moreover, in recent years, considerable evidence has been reported suggesting that upregulated glycolysis itself, through its enzymes and/or metabolites, may play a causative role in tumorigenesis, either by acting itself as an oncogenic stimulus or by facilitating the appearance of oncogenic mutations. In fact, several changes induced by upregulated glycolysis have been shown to be involved in tumor initiation and early tumorigenesis: glycolysis-induced chromatin remodeling, inhibition of premature senescence and induction of proliferation, effects on DNA repair, O-linked N-acetylglucosamine modification of target proteins, antiapoptotic effects, induction of epithelial–mesenchymal transition or autophagy, and induction of angiogenesis. In this article we summarize the evidence that upregulated glycolysis is involved in tumor initiation and, in the following, we propose a mechanistic model aimed at explaining how upregulated glycolysis may play such a role. |
format | Online Article Text |
id | pubmed-10137279 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-101372792023-04-28 On the Role of Glycolysis in Early Tumorigenesis—Permissive and Executioner Effects Marcucci, Fabrizio Rumio, Cristiano Cells Review Reprogramming energy production from mitochondrial respiration to glycolysis is now considered a hallmark of cancer. When tumors grow beyond a certain size they give rise to changes in their microenvironment (e.g., hypoxia, mechanical stress) that are conducive to the upregulation of glycolysis. Over the years, however, it has become clear that glycolysis can also associate with the earliest steps of tumorigenesis. Thus, many of the oncoproteins most commonly involved in tumor initiation and progression upregulate glycolysis. Moreover, in recent years, considerable evidence has been reported suggesting that upregulated glycolysis itself, through its enzymes and/or metabolites, may play a causative role in tumorigenesis, either by acting itself as an oncogenic stimulus or by facilitating the appearance of oncogenic mutations. In fact, several changes induced by upregulated glycolysis have been shown to be involved in tumor initiation and early tumorigenesis: glycolysis-induced chromatin remodeling, inhibition of premature senescence and induction of proliferation, effects on DNA repair, O-linked N-acetylglucosamine modification of target proteins, antiapoptotic effects, induction of epithelial–mesenchymal transition or autophagy, and induction of angiogenesis. In this article we summarize the evidence that upregulated glycolysis is involved in tumor initiation and, in the following, we propose a mechanistic model aimed at explaining how upregulated glycolysis may play such a role. MDPI 2023-04-10 /pmc/articles/PMC10137279/ /pubmed/37190033 http://dx.doi.org/10.3390/cells12081124 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 Marcucci, Fabrizio Rumio, Cristiano On the Role of Glycolysis in Early Tumorigenesis—Permissive and Executioner Effects |
title | On the Role of Glycolysis in Early Tumorigenesis—Permissive and Executioner Effects |
title_full | On the Role of Glycolysis in Early Tumorigenesis—Permissive and Executioner Effects |
title_fullStr | On the Role of Glycolysis in Early Tumorigenesis—Permissive and Executioner Effects |
title_full_unstemmed | On the Role of Glycolysis in Early Tumorigenesis—Permissive and Executioner Effects |
title_short | On the Role of Glycolysis in Early Tumorigenesis—Permissive and Executioner Effects |
title_sort | on the role of glycolysis in early tumorigenesis—permissive and executioner effects |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10137279/ https://www.ncbi.nlm.nih.gov/pubmed/37190033 http://dx.doi.org/10.3390/cells12081124 |
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