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Abstract
When DNA damage occurs, cells stop the cell cycle and DNA repair can take place. However, if DNA damage exceeds DNA repair capacities, cells undergo either apoptosis or senescence. These mechanisms preclude the proliferation of cells with heavily damaged DNA, thus protecting the organism against tumour development.
When individuals are exposed to stress, the hypothalamic-pituitary-adrenal (HPA) axis and the sympathetic- adrenal-medullary (SAM) system can be activated leading to secretion of corticosteroids and catecholamines, respectively. The influences of these stress-related hormones have been proposed to promote cellular senescence. But paradoxically, chronic stimulation of the HPA axis is associated with higher risk of developing cancer.
Focusing on the DNA damage response pathway, this review discusses whether stress hormones induce senescence or tumour progression or both and presents historical and recent data that might help resolve some of these controversies.
Keywords: Catecholamine, DNA damage response, glucocorticoids, cellular senescence, tumour progression.
Current Drug Targets
Title:Stress Hormone-Mediated DNA Damage Response -- Implications for Cellular Senescence and Tumour Progression
Volume: 17 Issue: 4
Author(s): María Moreno-Villanueva and Alexander Bürkle
Affiliation:
Keywords: Catecholamine, DNA damage response, glucocorticoids, cellular senescence, tumour progression.
Abstract: When DNA damage occurs, cells stop the cell cycle and DNA repair can take place. However, if DNA damage exceeds DNA repair capacities, cells undergo either apoptosis or senescence. These mechanisms preclude the proliferation of cells with heavily damaged DNA, thus protecting the organism against tumour development.
When individuals are exposed to stress, the hypothalamic-pituitary-adrenal (HPA) axis and the sympathetic- adrenal-medullary (SAM) system can be activated leading to secretion of corticosteroids and catecholamines, respectively. The influences of these stress-related hormones have been proposed to promote cellular senescence. But paradoxically, chronic stimulation of the HPA axis is associated with higher risk of developing cancer.
Focusing on the DNA damage response pathway, this review discusses whether stress hormones induce senescence or tumour progression or both and presents historical and recent data that might help resolve some of these controversies.
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Cite this article as:
Moreno-Villanueva María and Bürkle Alexander, Stress Hormone-Mediated DNA Damage Response -- Implications for Cellular Senescence and Tumour Progression, Current Drug Targets 2016; 17 (4) . https://dx.doi.org/10.2174/1389450116666151001113720
DOI https://dx.doi.org/10.2174/1389450116666151001113720 |
Print ISSN 1389-4501 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-5592 |
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