ROS homeostasis and metabolism: a dangerous liason in cancer cells
By E. Panieri, M. Santoro. Cell Death and Disease, 2016
1,055 citations recorded by the source corpus.
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.
Subfields: Cancer Research, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/1d1dc45affc9c015f343b0e7ff6f85898ef0d1ed
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Citations in the corpus
- Superoxide dismutases: Dual roles in controlling ROS damage and regulating ROS signaling (2018, neutral): “After transformation and during tumor maintenance, cancer cells must cope with toxic effects of high oxidative stress and potentially alter their redox homeostasis to support fast growth (Panieri and Santoro, 2016).”
- ROS Generation and Antioxidant Defense Systems in Normal and Malignant Cells (2019, background): “Changes in redox homeostasis contribute to cancer development and progression [54].”
- Reactive Oxygen Species Signaling and Oxidative Stress: Transcriptional Regulation and Evolution (2024, background): “These could potentially serve as novel molecular targets for antioxidants or genetic modifications in new therapeutic strategies to counter ROS-related diseases, such as aging, cancer, neurodegeneration and chronic chemical intoxication.”