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Metabolic Reprogramming and Signaling to Chromatin Modifications in Tumorigenesis


Díaz-Hirashi, Zyanya; Gao, Tian; Verdeguer, Francisco (2020). Metabolic Reprogramming and Signaling to Chromatin Modifications in Tumorigenesis. In: Serpa, Jacinta. Tumor Microenvironment : The Main Driver of Metabolic Adaptation. Cham: Springer, 225-241.

Abstract

Cellular proliferation relies on a high energetic status, replenished through nutrient intake, that leads to the production of biosynthetic material. A communication between the energetic levels and the control of gene expression is essential to engage in cell division. Multiple nutrient and metabolic sensing mechanisms in cells control transcriptional responses through cell signaling cascades that activate specific transcription factors associated with a concomitant regulation of the chromatin state. In addition to this canonical axis, gene expression could be directly influenced by the fluctuation of specific key intermediary metabolites of central metabolic pathways which are also donors or cofactors of histone and DNA modifications. This alternative axis represents a more direct connection between nutrients and the epigenome function. Cancer cells are highly energetically demanding to sustain proliferation. To reach their energetic demands, cancer cells rewire metabolic pathways. Recent discoveries show that perturbations of metabolic pathways in cancer cells have a direct impact on the epigenome. In this chapter, the interaction between metabolic driven changes of transcriptional programs in the context of tumorigenesis will be discussed.

Abstract

Cellular proliferation relies on a high energetic status, replenished through nutrient intake, that leads to the production of biosynthetic material. A communication between the energetic levels and the control of gene expression is essential to engage in cell division. Multiple nutrient and metabolic sensing mechanisms in cells control transcriptional responses through cell signaling cascades that activate specific transcription factors associated with a concomitant regulation of the chromatin state. In addition to this canonical axis, gene expression could be directly influenced by the fluctuation of specific key intermediary metabolites of central metabolic pathways which are also donors or cofactors of histone and DNA modifications. This alternative axis represents a more direct connection between nutrients and the epigenome function. Cancer cells are highly energetically demanding to sustain proliferation. To reach their energetic demands, cancer cells rewire metabolic pathways. Recent discoveries show that perturbations of metabolic pathways in cancer cells have a direct impact on the epigenome. In this chapter, the interaction between metabolic driven changes of transcriptional programs in the context of tumorigenesis will be discussed.

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Additional indexing

Item Type:Book Section, refereed, original work
Communities & Collections:05 Vetsuisse Faculty > Veterinärwissenschaftliches Institut > Department of Molecular Mechanisms of Disease
07 Faculty of Science > Department of Molecular Mechanisms of Disease
Dewey Decimal Classification:570 Life sciences; biology
Scopus Subject Areas:Life Sciences > General Biochemistry, Genetics and Molecular Biology
Language:English
Date:2020
Deposited On:16 Mar 2021 15:17
Last Modified:25 Jun 2024 01:38
Publisher:Springer
Series Name:Advances in Experimental Medicine and Biology
Number:1219
ISSN:0065-2598
ISBN:978-3-030-34024-7
OA Status:Closed
Publisher DOI:https://doi.org/10.1007/978-3-030-34025-4_12
PubMed ID:32130702