AMPK signaling and its targeting in cancer progression and treatment

The intrinsic mechanisms sensing the imbalance of energy in cells are pivotal for cell survival under various environmental insults. AMP-activated protein kinase (AMPK) serves as a central guardian maintaining energy homeostasis by orchestrating diverse cellular processes, such as lipogenesis, glyco...

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Bibliographic Details
Published inSeminars in cancer biology Vol. 85; pp. 52 - 68
Main Authors Hsu, Che-Chia, Peng, Danni, Cai, Zhen, Lin, Hui-Kuan
Format Journal Article
LanguageEnglish
Published England Elsevier Ltd 01.10.2022
Subjects
AMP-Activated Protein Kinases - metabolism
AMPK
Cancer
Energy Metabolism
Epigenesis, Genetic
Glucose deprivation
Humans
Metabolism
Mitocondria
Neoplasms - drug therapy
Neoplasms - metabolism
Phosphorylation
Signal Transduction
AMPK
Phosphorylation
Glucose deprivation
Metabolism
Cancer
Mitocondria
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Abstract The intrinsic mechanisms sensing the imbalance of energy in cells are pivotal for cell survival under various environmental insults. AMP-activated protein kinase (AMPK) serves as a central guardian maintaining energy homeostasis by orchestrating diverse cellular processes, such as lipogenesis, glycolysis, TCA cycle, cell cycle progression and mitochondrial dynamics. Given that AMPK plays an essential role in the maintenance of energy balance and metabolism, managing AMPK activation is considered as a promising strategy for the treatment of metabolic disorders such as type 2 diabetes and obesity. Since AMPK has been attributed to aberrant activation of metabolic pathways, mitochondrial dynamics and functions, and epigenetic regulation, which are hallmarks of cancer, targeting AMPK may open up a new avenue for cancer therapies. Although AMPK is previously thought to be involved in tumor suppression, several recent studies have unraveled its tumor promoting activity. The double-edged sword characteristics for AMPK as a tumor suppressor or an oncogene are determined by distinct cellular contexts. In this review, we will summarize recent progress in dissecting the upstream regulators and downstream effectors for AMPK, discuss the distinct roles of AMPK in cancer regulation and finally offer potential strategies with AMPK targeting in cancer therapy.
AbstractList The intrinsic mechanisms sensing the imbalance of energy in cells are pivotal for cell survival under various environmental insults. AMP-activated protein kinase (AMPK) serves as a central guardian maintaining energy homeostasis by orchestrating diverse cellular processes, such as lipogenesis, glycolysis, TCA cycle, cell cycle progression and mitochondrial dynamics. Given that AMPK plays an essential role in the maintenance of energy balance and metabolism, managing AMPK activation is considered as a promising strategy for the treatment of metabolic disorders such as type 2 diabetes and obesity. Since AMPK has been attributed to aberrant activation of metabolic pathways, mitochondrial dynamics and functions, and epigenetic regulation, which are hallmarks of cancer, targeting AMPK may open up a new avenue for cancer therapies. Although AMPK is previously thought to be involved in tumor suppression, several recent studies have unraveled its tumor promoting activity. The double-edged sword characteristics for AMPK as a tumor suppressor or an oncogene are determined by distinct cellular contexts. In this review, we will summarize recent progress in dissecting the upstream regulators and downstream effectors for AMPK, discuss the distinct roles of AMPK in cancer regulation and finally offer potential strategies with AMPK targeting in cancer therapy.
The intrinsic mechanisms sensing the imbalance of energy in cells are pivotal for cell survival under various environmental insults. AMP-activated protein kinase (AMPK) serves as a central guardian maintaining energy homeostasis by orchestrating diverse cellular processes, such as lipogenesis, glycolysis, TCA cycle, cell cycle progression and mitochondrial dynamics. Given that AMPK plays an essential role in the maintenance of energy balance and metabolism, managing AMPK activation is considered as a promising strategy for the treatment of metabolic disorders such as type 2 diabetes and obesity. Since AMPK has been attributed to aberrant activation of metabolic pathways, mitochondrial dynamics and functions, and epigenetic regulation, which are hallmarks of cancer, targeting AMPK may open up a new avenue for cancer therapies. Although AMPK is previously thought to be involved in tumor suppression, several recent studies have unraveled its tumor promoting activity. The double-edged sword characteristics for AMPK as a tumor suppressor or an oncogene are determined by distinct cellular contexts. In this review, we will summarize recent progress in dissecting the upstream regulators and downstream effectors for AMPK, discuss the distinct roles of AMPK in cancer regulation and finally offer potential strategies with AMPK targeting in cancer therapy.The intrinsic mechanisms sensing the imbalance of energy in cells are pivotal for cell survival under various environmental insults. AMP-activated protein kinase (AMPK) serves as a central guardian maintaining energy homeostasis by orchestrating diverse cellular processes, such as lipogenesis, glycolysis, TCA cycle, cell cycle progression and mitochondrial dynamics. Given that AMPK plays an essential role in the maintenance of energy balance and metabolism, managing AMPK activation is considered as a promising strategy for the treatment of metabolic disorders such as type 2 diabetes and obesity. Since AMPK has been attributed to aberrant activation of metabolic pathways, mitochondrial dynamics and functions, and epigenetic regulation, which are hallmarks of cancer, targeting AMPK may open up a new avenue for cancer therapies. Although AMPK is previously thought to be involved in tumor suppression, several recent studies have unraveled its tumor promoting activity. The double-edged sword characteristics for AMPK as a tumor suppressor or an oncogene are determined by distinct cellular contexts. In this review, we will summarize recent progress in dissecting the upstream regulators and downstream effectors for AMPK, discuss the distinct roles of AMPK in cancer regulation and finally offer potential strategies with AMPK targeting in cancer therapy.
Author Lin, Hui-Kuan
Peng, Danni
Cai, Zhen
Hsu, Che-Chia
AuthorAffiliation a Department of Cancer Biology, Wake Forest Baptist Medical Center, Wake Forest University, Winston-Salem, NC 27101, USA
AuthorAffiliation_xml – name: a Department of Cancer Biology, Wake Forest Baptist Medical Center, Wake Forest University, Winston-Salem, NC 27101, USA
Author_xml – sequence: 1
  givenname: Che-Chia
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  fullname: Peng, Danni
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  givenname: Zhen
  orcidid: 0000-0002-3736-4831
  surname: Cai
  fullname: Cai, Zhen
  email: zcai@wakehealth.edu
– sequence: 4
  givenname: Hui-Kuan
  orcidid: 0000-0002-3501-2410
  surname: Lin
  fullname: Lin, Hui-Kuan
  email: hulin@wakehealth.edu
BackLink https://www.ncbi.nlm.nih.gov/pubmed/33862221$$D View this record in MEDLINE/PubMed
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IngestDate Thu Aug 21 18:36:23 EDT 2025
Thu Jul 10 18:31:23 EDT 2025
Mon Jul 21 05:36:41 EDT 2025
Tue Jul 01 02:43:44 EDT 2025
Thu Apr 24 23:11:46 EDT 2025
Sun Apr 06 06:54:26 EDT 2025
Tue Aug 26 16:31:53 EDT 2025
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Keywords AMPK
Phosphorylation
Glucose deprivation
Metabolism
Cancer
Mitocondria
Language English
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Snippet The intrinsic mechanisms sensing the imbalance of energy in cells are pivotal for cell survival under various environmental insults. AMP-activated protein...
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SubjectTerms AMP-Activated Protein Kinases - metabolism
AMPK
Cancer
Energy Metabolism
Epigenesis, Genetic
Glucose deprivation
Humans
Metabolism
Mitocondria
Neoplasms - drug therapy
Neoplasms - metabolism
Phosphorylation
Signal Transduction
Title AMPK signaling and its targeting in cancer progression and treatment
URI https://www.clinicalkey.com/#!/content/1-s2.0-S1044579X21001073
https://dx.doi.org/10.1016/j.semcancer.2021.04.006
https://www.ncbi.nlm.nih.gov/pubmed/33862221
https://www.proquest.com/docview/2514598910
https://pubmed.ncbi.nlm.nih.gov/PMC9768867
Volume 85
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