Modulation of oxidative stress as an anticancer strategy

By C. Gorrini, I. Harris, T. Mak. Nature reviews. Drug discovery, 2013

3,257 citations recorded by the source corpus.

Subfields: Cancer Research, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/ac32eb49a02bacf6a017c23705573072987ff401

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cancer Research

1. Ralph J. Deberardinis
2. Navdeep S. Chandel
3. Brent R. Stockwell
4. C. V. Dang
5. E. Panieri
6. M. Santoro
7. Scott J. Dixon
8. Qing-zhang Tuo

In Molecular Biology

1. Brent R. Stockwell
2. Scott J. Dixon
3. Ralph J. Deberardinis
4. Navdeep S. Chandel
5. C. V. Dang
6. E. Panieri
7. M. Santoro
8. A. Dinkova-Kostova

Citations in the corpus

• ROS homeostasis and metabolism: a dangerous liason in cancer cells (2016, background): “The PPP is a major catabolic pathway of glucose through which cancer cells produce large amounts of ribose-5 phosphate, a precursor of nucleotide synthesis and NADPH, a key molecule that is used to drive anabolic processes and to detoxify harmful ROS.90 Activation of the PPP represents a key hallmar”
• Ferroptosis in cancer: from molecular mechanisms to therapeutic strategies (2024, background): “170 Stabilizing and overexpressing the anti-ferroptotic systems are crucial mechanisms evolved by tumor cells to avert ferroptosis and promote tumor progression.”
• The Roles of NRF2 in Modulating Cellular Iron Homeostasis (2017, background): “Excellent reviews encompassing the NRF2peroxiredoxin system are available (35, 39, 150, 174).”
• Pharmacological inhibition of cystine–glutamate exchange induces endoplasmic reticulum stress and ferroptosis (2014, background): “Consistent induction of ferroptosis in various cells under a variety of growth conditions Erastin and SAS were previously shown to trigger ferroptosis in human HT-1080 fibrosarcoma cells grown on two-dimensional substrates with atmospheric levels of oxygen (i.e., 21% oxygen) (Dixon et al., 2012).”
• Nrf2 inhibition reverses the resistance of cisplatin-resistant head and neck cancer cells to artesunate-induced ferroptosis (2016, background): “Indeed, Nrf2 is an oncogenic transcriptional factor that plays a key role against environmental or intracellular stress and controls the abundant cellular antioxidant systems responsible for GSH production in cancer cells [40].”
• Oxidative Stress in Cancer (2020, background): “Expression of SNAIL, SLUG, TWIST1, ZEB1, and ZEB2 is subject to complex control mechanisms, including transcriptional regulation by AP1, HIF-1α, NFκB, and TP53 (Figure 5B), a fact that implies that the ability of EMT-TFs to induce mesenchymal-related genes and repress epithelial-related genes is con”
• Transcriptional Regulation by Nrf2 (2017, background): “Cells normally counteract the detrimental effects of ROS and electrophiles through the activation of nuclear factor E2-related factor 2 (Nrf2; Nfe2l2 gene name) (42).”
• NAD+ metabolism: pathophysiologic mechanisms and therapeutic potential (2020, background): “The complex I and complex III of ETC are able to produce the superoxide anion radical (O2 –) and release it to both the matrix and the intermembrane space.114–116 Additionally, NADH or FADH2 is the electron carrier for the mitochondrial membrane proteins, such as GPDM and FQR, and the metabolic enzy”