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The neuroendocrine impact of chronic stress on cancer
Journal article   Open access   Peer reviewed

The neuroendocrine impact of chronic stress on cancer

Premal H Thaker, Susan K Lutgendorf and Anil K Sood
Cell cycle (Georgetown, Tex.), Vol.6(4), pp.430-433
02/15/2007
DOI: 10.4161/cc.6.4.3829
PMID: 17312398
url
https://doi.org/10.4161/cc.6.4.3829View
Published (Version of record) Open Access

Abstract

Behavioral processes have long been suspected to influence many health processes including effects on cancer. However, mechanisms underlying these observations are not fully understood. Recent work has demonstrated that chronic behavioral stress results in higher levels of tissue catecholamines, greater tumor burden, and a more invasive pattern of ovarian cancer growth in an orthotopic mouse model. These effects are mediated primarily through the beta(2) adrenergic receptor (ADRB2) activation of the tumor cell cyclic AMP (cAMP)-protein kinase A (PKA) signaling pathway. Additionally, tumors in stressed animals have increased vascularization and enhanced expression of vascular endothelial growth factor (VEGF) and matrix metalloproteinases (MMPs) -2 and -9. In this review, we highlight the importance of the neuroendocrine stress response in tumor biology and discuss mechanisms by which the beta-adrenergic receptors on ovarian cancer cells enhance angiogenesis and tumor growth.
Cyclic AMP-Dependent Protein Kinases - metabolism Receptors, Adrenergic, beta-2 - physiology Signal Transduction Matrix Metalloproteinase 2 - metabolism Humans Neovascularization, Pathologic Vascular Endothelial Growth Factor A - metabolism Carcinoma - etiology Cyclic AMP-Dependent Protein Kinases - physiology Matrix Metalloproteinase 9 - metabolism Animals Stress, Psychological - metabolism Neurosecretory Systems - metabolism Female Carcinoma - blood supply Mice Ovarian Neoplasms - metabolism Carcinoma - metabolism Ovarian Neoplasms - blood supply Ovarian Neoplasms - etiology Stress, Psychological - complications

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