Mitochondrial Plasticity and Glucose Metabolic Alterations in Human Cancer under Oxidative Stress-From Viewpoints of Chronic Inflammation and Neutrophil Extracellular Traps (NETs)

Oxidative stress elicited by reactive oxygen species (ROS) and chronic inflammation are involved both in deterring and the generation/progression of human cancers. Exogenous ROS can injure mitochondria and induce them to generate more endogenous mitochondrial ROS to further perpetuate the deteriorat...

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Bibliographic Details
Published in:International journal of molecular sciences 2024-08, Vol.25 (17), p.9458
Main Authors: Lee, Hui-Ting, Lin, Chen-Sung, Liu, Chao-Yu, Chen, Po, Tsai, Chang-Youh, Wei, Yau-Huei
Format: Article
Language:English
Subjects:
Dehydrogenases
Extracellular Traps - metabolism
Glucose
Glucose - metabolism
Humans
Inflammation
Inflammation - metabolism
Inflammation - pathology
Kinases
Liver cancer
Metabolism
Mitochondria
Mitochondria - metabolism
mitochondrial plasticity
Neoplasms - immunology
Neoplasms - metabolism
Neoplasms - pathology
neutrophil
neutrophil extracellular traps (NETs)
Neutrophils
Neutrophils - metabolism
Oxidation
Oxidative Stress
Phosphorylation
Protons
Reactive oxygen species
Reactive Oxygen Species - metabolism
Warburg effect
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Summary:Oxidative stress elicited by reactive oxygen species (ROS) and chronic inflammation are involved both in deterring and the generation/progression of human cancers. Exogenous ROS can injure mitochondria and induce them to generate more endogenous mitochondrial ROS to further perpetuate the deteriorating condition in the affected cells. Dysfunction of these cancer mitochondria may possibly be offset by the Warburg effect, which is characterized by amplified glycolysis and metabolic reprogramming. ROS from neutrophil extracellular traps (NETs) are an essential element for neutrophils to defend against invading pathogens or to kill cancer cells. A chronic inflammation typically includes consecutive NET activation and tissue damage, as well as tissue repair, and together with NETs, ROS would participate in both the destruction and progression of cancers. This review discusses human mitochondrial plasticity and the glucose metabolic reprogramming of cancer cells confronting oxidative stress by the means of chronic inflammation and neutrophil extracellular traps (NETs).
ISSN:1422-0067
1661-6596
1422-0067
DOI:10.3390/ijms25179458