Stress Hormone-Mediated DNA Damage Response -- Implications for Cellular Senescence and Tumour Progression

Author(s): María Moreno-Villanueva, Alexander Bürkle

Journal Name: Current Drug Targets

Volume 17 , Issue 4 , 2016

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Graphical 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.

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Article Details

Year: 2016
Published on: 01 October, 2015
Page: [398 - 404]
Pages: 7
DOI: 10.2174/1389450116666151001113720
Price: $65

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