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Critical role of AMPK in redox regulation under glucose starvation

Glucose starvation is one of the major forms of metabolic stress in cancer cells. Deprivation of glucose impairs glycolysis and the pentose phosphate pathway, which elicits oxidative stress due to enhanced production of reactive oxygen species (ROS) and impaired antioxidant system, leading to redox...

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Detalles Bibliográficos
Autores principales: Ren, Yi, Shen, Han-Ming
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6859544/
https://www.ncbi.nlm.nih.gov/pubmed/30853530
http://dx.doi.org/10.1016/j.redox.2019.101154
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author Ren, Yi
Shen, Han-Ming
author_facet Ren, Yi
Shen, Han-Ming
author_sort Ren, Yi
collection PubMed
description Glucose starvation is one of the major forms of metabolic stress in cancer cells. Deprivation of glucose impairs glycolysis and the pentose phosphate pathway, which elicits oxidative stress due to enhanced production of reactive oxygen species (ROS) and impaired antioxidant system, leading to redox imbalance and cell death. Under glucose starvation, the 5′ AMP-activated protein kinase (AMPK) plays a critical role in maintaining redox homeostasis and cell survival via multiple pathways, such as regulation of fatty acid metabolism and antioxidant response. Convergence of ROS and the glucose metabolic pathway reveals novel molecular targets for the development of effective cancer therapeutic strategies. Interestingly, AMPK, along with its upstream kinase liver kinase B1 (LKB1), has been regarded to play a tumor suppressor role. However, emerging studies have provided novel insights into the pro-tumor survival function of the LKB1-AMPK pathway. Therefore, targeting metabolic and oxidative stress in cancer cells, with manipulation of AMPK activity, is a promising strategy in developing novel cancer therapeutic agents.
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spelling pubmed-68595442019-11-22 Critical role of AMPK in redox regulation under glucose starvation Ren, Yi Shen, Han-Ming Redox Biol Article Glucose starvation is one of the major forms of metabolic stress in cancer cells. Deprivation of glucose impairs glycolysis and the pentose phosphate pathway, which elicits oxidative stress due to enhanced production of reactive oxygen species (ROS) and impaired antioxidant system, leading to redox imbalance and cell death. Under glucose starvation, the 5′ AMP-activated protein kinase (AMPK) plays a critical role in maintaining redox homeostasis and cell survival via multiple pathways, such as regulation of fatty acid metabolism and antioxidant response. Convergence of ROS and the glucose metabolic pathway reveals novel molecular targets for the development of effective cancer therapeutic strategies. Interestingly, AMPK, along with its upstream kinase liver kinase B1 (LKB1), has been regarded to play a tumor suppressor role. However, emerging studies have provided novel insights into the pro-tumor survival function of the LKB1-AMPK pathway. Therefore, targeting metabolic and oxidative stress in cancer cells, with manipulation of AMPK activity, is a promising strategy in developing novel cancer therapeutic agents. Elsevier 2019-03-02 /pmc/articles/PMC6859544/ /pubmed/30853530 http://dx.doi.org/10.1016/j.redox.2019.101154 Text en © 2019 The Authors http://creativecommons.org/licenses/by-nc-nd/4.0/ This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
spellingShingle Article
Ren, Yi
Shen, Han-Ming
Critical role of AMPK in redox regulation under glucose starvation
title Critical role of AMPK in redox regulation under glucose starvation
title_full Critical role of AMPK in redox regulation under glucose starvation
title_fullStr Critical role of AMPK in redox regulation under glucose starvation
title_full_unstemmed Critical role of AMPK in redox regulation under glucose starvation
title_short Critical role of AMPK in redox regulation under glucose starvation
title_sort critical role of ampk in redox regulation under glucose starvation
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6859544/
https://www.ncbi.nlm.nih.gov/pubmed/30853530
http://dx.doi.org/10.1016/j.redox.2019.101154
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