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Journal ArticleDOI

Modulation of oxidative stress as an anticancer strategy.

TLDR
The controversial role of ROS in tumour development and in responses to anticancer therapies is addressed, and the idea that targeting the antioxidant capacity of tumour cells can have a positive therapeutic impact is elaborate.
Abstract
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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Citations
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Journal ArticleDOI

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.
Journal ArticleDOI

Fundamentals of cancer metabolism

TL;DR: A conceptual framework to understand how and why metabolic reprogramming occurs in tumor cells, and the mechanisms linking altered metabolism to tumorigenesis and metastasis will progressively support the development of new strategies to treat human cancer.
Journal ArticleDOI

ROS Are Good.

TL;DR: This Opinion focuses on the possibility that ROS are beneficial to plants, supporting cellular proliferation, physiological function, and viability, and that maintaining a basal level of ROS in cells is essential for life.
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

Cellular mechanisms and physiological consequences of redox-dependent signalling

TL;DR: The sources of ROS within cells and what is known regarding how intracellular oxidant levels are regulated are discussed, with the recent observations that reduction–oxidation (redox)-dependent regulation has a crucial role in an ever-widening range of biological activities.
References
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Journal ArticleDOI

Hallmarks of cancer: the next generation.

TL;DR: Recognition of the widespread applicability of these concepts will increasingly affect the development of new means to treat human cancer.
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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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Ferroptosis: An Iron-Dependent Form of Nonapoptotic Cell Death

TL;DR: This paper identified the small molecule ferrostatin-1 as a potent inhibitor of ferroptosis in cancer cells and glutamate-induced cell death in organotypic rat brain slices, suggesting similarities between these two processes.
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Akt Promotes Cell Survival by Phosphorylating and Inhibiting a Forkhead Transcription Factor

TL;DR: It is demonstrated that Akt also regulates the activity of FKHRL1, a member of the Forkhead family of transcription factors, which triggers apoptosis most likely by inducing the expression of genes that are critical for cell death, such as the Fas ligand gene.
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