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ROS homeostasis and metabolism: a dangerous liason in cancer cells.

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TLDR
How the mitochondria has a key role in regulating the interplay between redox homeostasis and metabolism within tumor cells is described, and the potential therapeutic use of agents that directly or indirectly block metabolism is discussed.
Abstract
Tumor cells harbor genetic alterations that promote a continuous and elevated production of reactive oxygen species. Whereas such oxidative stress conditions would be harmful to normal cells, they facilitate tumor growth in multiple ways by causing DNA damage and genomic instability, and ultimately, by reprogramming cancer cell metabolism. This review outlines the metabolic-dependent mechanisms that tumors engage in when faced with oxidative stress conditions that are critical for cancer progression by producing redox cofactors. In particular, we describe how the mitochondria has a key role in regulating the interplay between redox homeostasis and metabolism within tumor cells. Last, we will discuss the potential therapeutic use of agents that directly or indirectly block metabolism.

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Journal ArticleDOI

Reactive oxygen species (ROS) as pleiotropic physiological signalling agents.

TL;DR: This work focuses on ROS at physiological levels and their central role in redox signalling via different post-translational modifications, denoted as ‘oxidative eustress’.
Journal ArticleDOI

ROS signalling in the biology of cancer.

TL;DR: The generation and sources of ROS within tumour cells, the regulation of ROS by antioxidant defence systems, as well as the effect of elevated ROS production on their signalling targets in cancer are discussed.
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ROS in cancer therapy: the bright side of the moon

TL;DR: The review will emphasize the molecular mechanisms useful for the development of therapeutic strategies that are based on modulating ROS levels to treat cancer, and report on the growing data that highlight the role of ROS generated by different metabolic pathways as Trojan horses to eliminate cancer cells.
Journal ArticleDOI

Superoxide dismutases: Dual roles in controlling ROS damage and regulating ROS signaling.

TL;DR: Studies in model organisms and humans are discussed, which reveal the dual roles of SOD enzymes in controlling damage and regulating signaling and the need for fine local control of ROS signaling.
Journal ArticleDOI

ROS Generation and Antioxidant Defense Systems in Normal and Malignant Cells

TL;DR: This review covers the current data on the mechanisms of ROS generation and existing antioxidant systems balancing the redox state in mammalian cells that can also be related to tumors.
References
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Journal ArticleDOI

A Model of Redox Kinetics Implicates the Thiol Proteome in Cellular Hydrogen Peroxide Responses

TL;DR: A network model of H( 2)O(2) clearance that includes the pseudo-enzymatic oxidative turnover of protein thiols, the enzymatic actions of catalase, glutathione peroxidase, peroxiredoxins, and glutaredoxin, and the redox reactions of thioredoxin and glutathionylated adducts is introduced.
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Gain of Nrf2 Function in Non-Small-Cell Lung Cancer Cells Confers Radioresistance

TL;DR: It is established that constitutive activation of Nrf2 protects against ionizing radiation toxicity and confers radioresistance, and targeting NRF2 activity in radioresistant tumors could be a promising strategy to circumvent radiores resistance.
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Glutaminase Isoenzymes as Key Regulators in Metabolic and Oxidative Stress Against Cancer

TL;DR: Modulation of GA function may be a new therapeutic target for cancer treatment after it was demonstrated to be regulated by oncogenes and to support tumor cell growth.
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Mitochondrial respiratory complex I dysfunction promotes tumorigenesis through ROS alteration and AKT activation

TL;DR: It is reported that the tumorigenic phenotype associated with complex I dysfunction could be reversed by introducing a yeast NADH quinone oxidoreductase (NDI1) gene, which bypassed the defective complex I and restored oxidative phosphorylation in the host cells.
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The Antioxidant Transcription Factor Nrf2 Negatively Regulates Autophagy and Growth Arrest Induced by the Anticancer Redox Agent Mitoquinone

TL;DR: MitoQ treatment led to irreversible inhibition of clonogenic growth of breast cancer cells through a combination of autophagy and apoptotic cell death mechanisms and should be further evaluated for novel anticancer activity.
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