Redox Homeostasis and Metabolism in Cancer: A Complex Mechanism and Potential Targeted Therapeutics.
Animals
Antineoplastic Agents
/ pharmacology
Clinical Trials as Topic
Disease Progression
Homeostasis
/ drug effects
Humans
Metabolic Networks and Pathways
/ drug effects
Molecular Targeted Therapy
Neoplasms
/ drug therapy
Oxidative Stress
/ drug effects
Reactive Oxygen Species
/ metabolism
Signal Transduction
/ drug effects
HIF-1α
Nrf2
PGC-1α
ROS
metabolic targeting
metabolism
oxidative stress
redox systems
Journal
International journal of molecular sciences
ISSN: 1422-0067
Titre abrégé: Int J Mol Sci
Pays: Switzerland
ID NLM: 101092791
Informations de publication
Date de publication:
28 Apr 2020
28 Apr 2020
Historique:
received:
24
02
2020
revised:
22
04
2020
accepted:
26
04
2020
entrez:
2
5
2020
pubmed:
2
5
2020
medline:
3
2
2021
Statut:
epublish
Résumé
Reactive Oxygen Species or "ROS" encompass several molecules derived from oxygen that can oxidize other molecules and subsequently transition rapidly between species. The key roles of ROS in biological processes are cell signaling, biosynthetic processes, and host defense. In cancer cells, increased ROS production and oxidative stress are instigated by carcinogens, oncogenic mutations, and importantly, metabolic reprograming of the rapidly proliferating cancer cells. Increased ROS production activates myriad downstream survival pathways that further cancer progression and metastasis. In this review, we highlight the relation between ROS, the metabolic programing of cancer, and stromal and immune cells with emphasis on and the transcription machinery involved in redox homeostasis, metabolic programing and malignant phenotype. We also shed light on the therapeutic targeting of metabolic pathways generating ROS as we investigate: Orlistat, Biguandes, AICAR, 2 Deoxyglucose, CPI-613, and Etomoxir.
Identifiants
pubmed: 32354000
pii: ijms21093100
doi: 10.3390/ijms21093100
pmc: PMC7247161
pii:
doi:
Substances chimiques
Antineoplastic Agents
0
Reactive Oxygen Species
0
Types de publication
Journal Article
Review
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : NIGMS NIH HHS
ID : T32 GM127261
Pays : United States
Organisme : NIH HHS
ID : T32GM127261
Pays : United States
Organisme : NIH HHS
ID : R01CA193437
Pays : United States
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