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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

The insulin and insulin-like growth factor receptor family in neoplasia: an update

TL;DR: Clinical studies may benefit from the use of predictive biomarkers to identify probable responders, theUse of rational combination therapies and the consideration of alternative targeting strategies, such as ligand-specific antibodies and receptor-specific tyrosine kinase inhibitors.
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AMPK regulates NADPH homeostasis to promote tumour cell survival during energy stress

TL;DR: It is shown that AMPK activation, during energy stress, prolongs cell survival by redox regulation and has a key function in NADPH maintenance, which is critical for cancer cell survival under energy stress conditions, such as glucose limitations, anchorage-independent growth and solid tumour formation in vivo.
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Cancer metabolism: fatty acid oxidation in the limelight

TL;DR: The important contribution of fatty acid oxidation to cancer cell function is brought to light in this Progress article.
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Glucose-Independent Glutamine Metabolism via TCA Cycling for Proliferation and Survival in B Cells

TL;DR: The metabolic responses of a MYC-inducible human Burkitt lymphoma model P493 cell line to aerobic and hypoxic conditions, and to glucose deprivation, are determined using stable isotope-resolved metabolomics to demonstrate an alternative energy-generating glutaminolysis pathway involving a glucose-independent TCA cycle.
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