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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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Biomimetic Activator of Sonodynamic Ferroptosis Amplifies Inherent Peroxidation for Improving the Treatment of Breast Cancer.

TL;DR: It is identified that SAFE, under ultrasound stimulation, can not only substantially supply oxygen to overcome tumor hypoxia associated therapeutic resistance, but effectively activate ferroptosis through the coeffect of SDT triggered ROS production and DGLA mediated lipid peroxidation.
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Manipulation of Glucose and Hydroperoxide Metabolism to Improve Radiation Response.

TL;DR: Preclinical and clinical data for targeting glucose and hydroperoxide metabolism in cancer suggest dual targeting of glycolysis and redox metabolism in combination with chemotherapy and radiation should be further evaluated in clinical trials.
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Extremely Low-Frequency Magnetic Fields and Redox-Responsive Pathways Linked to Cancer Drug Resistance: Insights from Co-Exposure-Based In Vitro Studies

TL;DR: This review builds a framework around how the activity of redox-responsive mediators may be controlled by co-exposure to ELF-MF and reactive oxygen species-generating agents in tumor and cancer cells, in order to clarify whether and how such potential molecular targets could help to minimize or neutralize the functional interaction between ELF -MF and malignancies.
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Reactive oxygen species in cancer: a paradox between pro- and anti-tumour activities

TL;DR: A revision of the current research about molecular aspects proposed to be involved in the anticancer features of oxidant and antioxidant-based therapies targeting cancer cells, and their participation in the balance of oxidative species and cancer cell death is presented.
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ROS-Dependent ER Stress and Autophagy Mediate the Anti-Tumor Effects of Tributyltin (IV) Ferulate in Colon Cancer Cells

TL;DR: Results indicate that ROS-dependent ER stress and autophagy play a major role in the TBT-F action mechanism in colon cancer cells and open a new perspective to consider the compound as a potential candidate for colon cancer treatment.
References
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Journal ArticleDOI

Understanding the Warburg Effect: The Metabolic Requirements of Cell Proliferation

TL;DR: It is proposed that the metabolism of cancer cells, and indeed all proliferating cells, is adapted to facilitate the uptake and incorporation of nutrients into the biomass needed to produce a new cell.
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ROS Function in Redox Signaling and Oxidative Stress

TL;DR: It is argued that redox biology, rather than oxidative stress, underlies physiological and pathological conditions.
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Regulation of cancer cell metabolism

TL;DR: Interest in the topic of tumour metabolism has waxed and waned over the past century, but it has become clear that many of the signalling pathways that are affected by genetic mutations and the tumour microenvironment have a profound effect on core metabolism, making this topic once again one of the most intense areas of research in cancer biology.
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Regulation of Ferroptotic Cancer Cell Death by GPX4

TL;DR: Targeted metabolomic profiling and chemoproteomics revealed that GPX4 is an essential regulator of ferroptotic cancer cell death and sensitivity profiling in 177 cancer cell lines revealed that diffuse large B cell lymphomas and renal cell carcinomas are particularly susceptible to GPx4-regulated ferroPTosis.
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Reactive oxygen species (ROS) homeostasis and redox regulation in cellular signaling

TL;DR: This review focuses on the molecular mechanisms through which ROS directly interact with critical signaling molecules to initiate signaling in a broad variety of cellular processes, such as proliferation and survival, ROS homeostasis and antioxidant gene regulation, mitochondrial oxidative stress, apoptosis, and aging.
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