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Metabolism and Brain Cancer
Cellular energy metabolism is one of the main processes affected during the transition from normal to cancer cells, and it is a crucial determinant of cell proliferation or cell death. As a support for rapid proliferation, cancer cells choose to use glycolysis even in the presence of oxygen (Warburg...
Autores principales: | , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo
2011
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3118436/ https://www.ncbi.nlm.nih.gov/pubmed/21779721 http://dx.doi.org/10.1590/S1807-59322011001300005 |
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author | Marie, Suely Kazue Nagahashi Shinjo, Sueli Mieko Oba |
author_facet | Marie, Suely Kazue Nagahashi Shinjo, Sueli Mieko Oba |
author_sort | Marie, Suely Kazue Nagahashi |
collection | PubMed |
description | Cellular energy metabolism is one of the main processes affected during the transition from normal to cancer cells, and it is a crucial determinant of cell proliferation or cell death. As a support for rapid proliferation, cancer cells choose to use glycolysis even in the presence of oxygen (Warburg effect) to fuel macromolecules for the synthesis of nucleotides, fatty acids, and amino acids for the accelerated mitosis, rather than fuel the tricarboxylic acid cycle and oxidative phosphorylation. Mitochondria biogenesis is also reprogrammed in cancer cells, and the destiny of those cells is determined by the balance between energy and macromolecule supplies, and the efficiency of buffering of the cumulative radical oxygen species. In glioblastoma, the most frequent and malignant adult brain tumor, a metabolic shift toward aerobic glycolysis is observed, with regulation by well known genes as integrants of oncogenic pathways such as phosphoinositide 3-kinase/protein kinase, MYC, and hypoxia regulated gene as hypoxia induced factor 1. The expression profile of a set of genes coding for glycolysis and the tricarboxylic acid cycle in glioblastoma cases confirms this metabolic switch. An understanding of how the main metabolic pathways are modified by cancer cells and the interactions between oncogenes and tumor suppressor genes with these pathways may enlighten new strategies in cancer therapy. In the present review, the main metabolic pathways are compared in normal and cancer cells, and key regulations by the main oncogenes and tumor suppressor genes are discussed. Potential therapeutic targets of the cancer energetic metabolism are enumerated, highlighting the astrocytomas, the most common brain cancer. |
format | Online Article Text |
id | pubmed-3118436 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2011 |
publisher | Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo |
record_format | MEDLINE/PubMed |
spelling | pubmed-31184362011-06-22 Metabolism and Brain Cancer Marie, Suely Kazue Nagahashi Shinjo, Sueli Mieko Oba Clinics (Sao Paulo) Editorial Cellular energy metabolism is one of the main processes affected during the transition from normal to cancer cells, and it is a crucial determinant of cell proliferation or cell death. As a support for rapid proliferation, cancer cells choose to use glycolysis even in the presence of oxygen (Warburg effect) to fuel macromolecules for the synthesis of nucleotides, fatty acids, and amino acids for the accelerated mitosis, rather than fuel the tricarboxylic acid cycle and oxidative phosphorylation. Mitochondria biogenesis is also reprogrammed in cancer cells, and the destiny of those cells is determined by the balance between energy and macromolecule supplies, and the efficiency of buffering of the cumulative radical oxygen species. In glioblastoma, the most frequent and malignant adult brain tumor, a metabolic shift toward aerobic glycolysis is observed, with regulation by well known genes as integrants of oncogenic pathways such as phosphoinositide 3-kinase/protein kinase, MYC, and hypoxia regulated gene as hypoxia induced factor 1. The expression profile of a set of genes coding for glycolysis and the tricarboxylic acid cycle in glioblastoma cases confirms this metabolic switch. An understanding of how the main metabolic pathways are modified by cancer cells and the interactions between oncogenes and tumor suppressor genes with these pathways may enlighten new strategies in cancer therapy. In the present review, the main metabolic pathways are compared in normal and cancer cells, and key regulations by the main oncogenes and tumor suppressor genes are discussed. Potential therapeutic targets of the cancer energetic metabolism are enumerated, highlighting the astrocytomas, the most common brain cancer. Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo 2011-06 /pmc/articles/PMC3118436/ /pubmed/21779721 http://dx.doi.org/10.1590/S1807-59322011001300005 Text en Copyright © 2011 Hospital das Clínicas da FMUSP http://creativecommons.org/licenses/by-nc/3.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Editorial Marie, Suely Kazue Nagahashi Shinjo, Sueli Mieko Oba Metabolism and Brain Cancer |
title | Metabolism and Brain Cancer |
title_full | Metabolism and Brain Cancer |
title_fullStr | Metabolism and Brain Cancer |
title_full_unstemmed | Metabolism and Brain Cancer |
title_short | Metabolism and Brain Cancer |
title_sort | metabolism and brain cancer |
topic | Editorial |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3118436/ https://www.ncbi.nlm.nih.gov/pubmed/21779721 http://dx.doi.org/10.1590/S1807-59322011001300005 |
work_keys_str_mv | AT mariesuelykazuenagahashi metabolismandbraincancer AT shinjosuelimiekooba metabolismandbraincancer |