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The Glycolytic Switch in Tumors: How Many Players Are Involved?

Reprogramming of cellular metabolism is a hallmark of cancers. Cancer cells more readily use glycolysis, an inefficient metabolic pathway for energy metabolism, even when sufficient oxygen is available. This reliance on aerobic glycolysis is called the Warburg effect, and promotes tumorigenesis and...

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Detalles Bibliográficos
Autores principales: Yu, Li, Chen, Xun, Sun, Xueqi, Wang, Liantang, Chen, Shangwu
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Ivyspring International Publisher 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5687156/
https://www.ncbi.nlm.nih.gov/pubmed/29151926
http://dx.doi.org/10.7150/jca.21125
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author Yu, Li
Chen, Xun
Sun, Xueqi
Wang, Liantang
Chen, Shangwu
author_facet Yu, Li
Chen, Xun
Sun, Xueqi
Wang, Liantang
Chen, Shangwu
author_sort Yu, Li
collection PubMed
description Reprogramming of cellular metabolism is a hallmark of cancers. Cancer cells more readily use glycolysis, an inefficient metabolic pathway for energy metabolism, even when sufficient oxygen is available. This reliance on aerobic glycolysis is called the Warburg effect, and promotes tumorigenesis and malignancy progression. The mechanisms of the glycolytic shift in tumors are not fully understood. Growing evidence demonstrates that many signal molecules, including oncogenes and tumor suppressors, are involved in the process, but how oncogenic signals attenuate mitochondrial function and promote the switch to glycolysis remains unclear. Here, we summarize the current information on several main mediators and discuss their possible mechanisms for triggering the Warburg effect.
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spelling pubmed-56871562017-11-18 The Glycolytic Switch in Tumors: How Many Players Are Involved? Yu, Li Chen, Xun Sun, Xueqi Wang, Liantang Chen, Shangwu J Cancer Review Reprogramming of cellular metabolism is a hallmark of cancers. Cancer cells more readily use glycolysis, an inefficient metabolic pathway for energy metabolism, even when sufficient oxygen is available. This reliance on aerobic glycolysis is called the Warburg effect, and promotes tumorigenesis and malignancy progression. The mechanisms of the glycolytic shift in tumors are not fully understood. Growing evidence demonstrates that many signal molecules, including oncogenes and tumor suppressors, are involved in the process, but how oncogenic signals attenuate mitochondrial function and promote the switch to glycolysis remains unclear. Here, we summarize the current information on several main mediators and discuss their possible mechanisms for triggering the Warburg effect. Ivyspring International Publisher 2017-09-20 /pmc/articles/PMC5687156/ /pubmed/29151926 http://dx.doi.org/10.7150/jca.21125 Text en © Ivyspring International Publisher This is an open access article distributed under the terms of the Creative Commons Attribution (CC BY-NC) license (https://creativecommons.org/licenses/by-nc/4.0/). See http://ivyspring.com/terms for full terms and conditions.
spellingShingle Review
Yu, Li
Chen, Xun
Sun, Xueqi
Wang, Liantang
Chen, Shangwu
The Glycolytic Switch in Tumors: How Many Players Are Involved?
title The Glycolytic Switch in Tumors: How Many Players Are Involved?
title_full The Glycolytic Switch in Tumors: How Many Players Are Involved?
title_fullStr The Glycolytic Switch in Tumors: How Many Players Are Involved?
title_full_unstemmed The Glycolytic Switch in Tumors: How Many Players Are Involved?
title_short The Glycolytic Switch in Tumors: How Many Players Are Involved?
title_sort glycolytic switch in tumors: how many players are involved?
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5687156/
https://www.ncbi.nlm.nih.gov/pubmed/29151926
http://dx.doi.org/10.7150/jca.21125
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