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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...

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Detalles Bibliográficos
Autores principales: Marcucci, Fabrizio, Rumio, Cristiano
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2023
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.
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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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