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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Published inRedox biology Vol. 25; p. 101154
Main Authors Ren, Yi, Shen, Han-Ming
Format Journal Article
LanguageEnglish
Published Netherlands Elsevier B.V 01.07.2019
Elsevier
Subjects
AMP-Activated Protein Kinases - metabolism
AMPK
Animals
Cancer
Fatty acid metabolism
Glucose - deficiency
Glucose metabolism
Humans
Neoplasms - enzymology
Neoplasms - pathology
Oxidation-Reduction
Oxidative Stress
Reactive oxygen species
Reactive Oxygen Species - metabolism
G-6P
HK
MTP
PTEN
KEAP1
OXPHOS
HIF-1α
IDH
6P-G
ERK2
PI3K
PPAR
TRIM28
CPT1
ME
mTOR
SCD1
Trx
G6PD
SREBP
Fatty acid metabolism
TSC2
CaMKKβ
MAPK
6PGD
GPx
MEF
RAPTOR
MEK
PDAC
R-5P
TCA
ARE
2DG
CRC
NOX
CAT
ROS
AMPK
AICAR
ULK1
DHA
GAPDH
mTORC1
CRM
NADPH
Reactive oxygen species
2DG-6P
COX-2
HO-1
LKB1
Glucose metabolism
PPP
NADH
NRF2
α-KG
UCP2
NADP
MAGE A3/6
GSH
6P-2DG
ACC
GLUT1
GSSG
NQO1
KO
NSCLC
SGLT2
5TG
SOD
3PG
BRAF
FADH2
PGC-1α
GR
ECM
NAC
ETC
FAO
FASN
FAS
UBE2O
KRAS
TP
HNE
Cancer
Glc
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Abstract 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.
AbstractList 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.
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.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.
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. Keywords: Reactive oxygen species, Glucose metabolism, Fatty acid metabolism, AMPK, Cancer
ArticleNumber 101154
Author Ren, Yi
Shen, Han-Ming
AuthorAffiliation Department of Physiology, Yong Loo Lin School of Medicine, National University of Singapore, 117593, Singapore
AuthorAffiliation_xml – name: Department of Physiology, Yong Loo Lin School of Medicine, National University of Singapore, 117593, Singapore
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  surname: Ren
  fullname: Ren, Yi
– sequence: 2
  givenname: Han-Ming
  surname: Shen
  fullname: Shen, Han-Ming
  email: phsshm@nus.edu.sg
BackLink https://www.ncbi.nlm.nih.gov/pubmed/30853530$$D View this record in MEDLINE/PubMed
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Keywords G-6P
HK
MTP
PTEN
KEAP1
OXPHOS
HIF-1α
IDH
6P-G
ERK2
PI3K
PPAR
TRIM28
CPT1
ME
mTOR
SCD1
Trx
G6PD
SREBP
Fatty acid metabolism
TSC2
CaMKKβ
MAPK
6PGD
GPx
MEF
RAPTOR
MEK
PDAC
R-5P
TCA
ARE
2DG
CRC
NOX
CAT
ROS
AMPK
AICAR
ULK1
DHA
GAPDH
mTORC1
CRM
NADPH
Reactive oxygen species
2DG-6P
COX-2
HO-1
LKB1
Glucose metabolism
PPP
NADH
NRF2
α-KG
UCP2
NADP
MAGE A3/6
GSH
6P-2DG
ACC
GLUT1
GSSG
NQO1
KO
NSCLC
SGLT2
5TG
SOD
3PG
BRAF
FADH2
PGC-1α
GR
ECM
NAC
ETC
FAO
FASN
FAS
UBE2O
KRAS
TP
HNE
Cancer
Glc
Language English
License This is an open access article under the CC BY-NC-ND license.
Copyright © 2019 The Authors. Published by Elsevier B.V. All rights reserved.
This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
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  year: 2019
  text: 2019-07-01
  day: 01
PublicationDecade 2010
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PublicationTitle Redox biology
PublicationTitleAlternate Redox Biol
PublicationYear 2019
Publisher Elsevier B.V
Elsevier
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Snippet Glucose starvation is one of the major forms of metabolic stress in cancer cells. Deprivation of glucose impairs glycolysis and the pentose phosphate pathway,...
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StartPage 101154
SubjectTerms AMP-Activated Protein Kinases - metabolism
AMPK
Animals
Cancer
Fatty acid metabolism
Glucose - deficiency
Glucose metabolism
Humans
Neoplasms - enzymology
Neoplasms - pathology
Oxidation-Reduction
Oxidative Stress
Reactive oxygen species
Reactive Oxygen Species - metabolism
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  providerName: Elsevier
Title Critical role of AMPK in redox regulation under glucose starvation
URI https://dx.doi.org/10.1016/j.redox.2019.101154
https://www.ncbi.nlm.nih.gov/pubmed/30853530
https://www.proquest.com/docview/2190118267
https://pubmed.ncbi.nlm.nih.gov/PMC6859544
https://doaj.org/article/042e5c48b1084c159e907bb0f112edad
Volume 25
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