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Title:
Modulation of oxidative stress as an anticancer strategy | Nature Reviews Drug Discovery
Description:
Cancer cells have high levels of reactive oxygen species (ROS) owing to metabolic and genetic alterations. The role of ROS in cancer cells is controversial as they can have both pro-tumorigenic and antitumorigenic properties. In this Review, Mak and colleagues discuss recent findings that cancer cells upregulate antioxidant pathways to counteract ROS, and explore the potential of anticancer strategies that target the antioxidant capacity of tumour cells. The regulation of oxidative stress is an important factor in both tumour development and responses to anticancer therapies. Many signalling pathways that are linked to tumorigenesis can also regulate the metabolism of reactive oxygen species (ROS) through direct or indirect mechanisms. High ROS levels are generally detrimental to cells, and the redox status of cancer cells usually differs from that of normal cells. Because of metabolic and signalling aberrations, cancer cells exhibit elevated ROS levels. The observation that this is balanced by an increased antioxidant capacity suggests that high ROS levels may constitute a barrier to tumorigenesis. However, ROS can also promote tumour formation by inducing DNA mutations and pro-oncogenic signalling pathways. These contradictory effects have important implications for potential anticancer strategies that aim to modulate levels of ROS. In this Review, we address the controversial role of ROS in tumour development and in responses to anticancer therapies, and elaborate on the idea that targeting the antioxidant capacity of tumour cells can have a positive therapeutic impact.
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30 years and 10 months (reg. 1994-08-11).
Title:
Modulation of oxidative stress as an anticancer strategy | Nature Reviews Drug Discovery
Description:
Cancer cells have high levels of reactive oxygen species (ROS) owing to metabolic and genetic alterations. The role of ROS in cancer cells is controversial as they can have both pro-tumorigenic and antitumorigenic properties. In this Review, Mak and colleagues discuss recent findings that cancer cells upregulate antioxidant pathways to counteract ROS, and explore the potential of anticancer strategies that target the antioxidant capacity of tumour cells. The regulation of oxidative stress is an important factor in both tumour development and responses to anticancer therapies. Many signalling pathways that are linked to tumorigenesis can also regulate the metabolism of reactive oxygen species (ROS) through direct or indirect mechanisms. High ROS levels are generally detrimental to cells, and the redox status of cancer cells usually differs from that of normal cells. Because of metabolic and signalling aberrations, cancer cells exhibit elevated ROS levels. The observation that this is balanced by an increased antioxidant capacity suggests that high ROS levels may constitute a barrier to tumorigenesis. However, ROS can also promote tumour formation by inducing DNA mutations and pro-oncogenic signalling pathways. These contradictory effects have important implications for potential anticancer strategies that aim to modulate levels of ROS. In this Review, we address the controversial role of ROS in tumour development and in responses to anticancer therapies, and elaborate on the idea that targeting the antioxidant capacity of tumour cells can have a positive therapeutic impact.
Website Age:
30 years and 10 months (reg. 1994-08-11).
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Keywords {π}
pubmed, article, google, scholar, cas, cancer, central, cell, nature, cells, stress, oxidative, oxygen, ros, biol, res, species, med, reactive, antioxidant, redox, metabolism, nrf, apoptosis, regulation, signaling, levels, tumor, mitochondrial, biochem, transcription, inhibition, science, response, natl, tumour, factor, rev, survival, gene, sci, role, dna, signal, mol, breast, drug, death, mutations, chem,
Topics {βοΈ}
scientific editing permissions reprints nature portfolio privacy policy breast cancer research cap'n'collar transcription factor advertising health research b-cell-specific transcription factor social media dna cross-linking agents research tamoxifen-resistant mcf-7 cells p66shc-dependent signaling pathway xc- cystine/glutamate antiporter triple-negative breast cancer hypoxia-induced cellular responses plasma l-asparagine starvation amplify ros-dependent signaling cancer-initiating cell profit glucose-6-phosphate dehydrogenase activity pax3-fkhr fusion protein brca1-deficient mammary tumors tumour-specific gene alteration egfr-akt axis results oncogene-induced genetic instability Ξ²-catenin confers resistance phosphate-activated glutaminase keap1-cul3 e3 ligase pro-oncogenic signalling pathways serine/threonine kinase akt oxidative stress marker genotype-selective antitumor agents specific vitamin/mineral combinations c-myc potentiate apoptosis personal data author correspondence caspase-independent cell death nature cell biol anti-inflammatory drug mediates survival signaling inducing ros-mediated apoptosis data protection springerlink instant access oxidative stress-mediated homeostasis permissions foxo transcription factors forkhead transcription factor nrf2-regulated genes induced reactive oxygen species
Questions {β}
- CD44: can a cancer-initiating cell profit from an abundantly expressed molecule?
- Endoplasmic reticulum stress and oxidative stress: a vicious cycle or a double-edged sword?
- Hsp90 molecular chaperone inhibitors: are we there yet?
- Targeting cancer cells by ROS-mediated mechanisms: a radical therapeutic approach?
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