Journal
PSYCHONEUROENDOCRINOLOGY
Volume 99, Issue -, Pages 191-195Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.psyneuen.2018.09.012
Keywords
Epinephrine; Norepinephrine; Cancer; Stress-enhanced metastasis; Splanchnic nerve; Inflammatory reflex
Categories
Funding
- National Breast Cancer Foundation Australia postdoctoral fellowship [PF-15-014]
- Monash Interdisciplinary Research Scheme Award
- David and Lorelle Skewes Foundation
- Peter Mac Foundation
- National Health and Medical Research Council [APP1147498, APP1098887]
- NHMRC [APP1042492]
- Victorian Government's Operational Infrastructure Support Program
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Signaling through beta-adrenergic receptors drives cancer progression and beta-blockers are being evaluated as a novel therapeutic strategy to prevent metastasis. Orthotopic mouse models of breast cancer show that beta-adrenergic signaling induced by chronic stress accelerates metastasis, and that beta(2)-adrenergic receptors on tumor cells are critical for this. Endogenous catecholamines are released during chronic stress: norepinephrine from the adrenal medulla and sympathetic nerves, and epinephrine from the adrenal medulla. beta(2)-adrenergic receptors are much more sensitive to epinephrine than to norepinephrine. To determine if epinephrine is necessary in the effects of stress on cancer progression, we used a denervation strategy to eliminate circulating epinephrine, and quantified the effect on metastasis. Using both human xenograft and immune-intact murine models of breast cancer, we show that circulating epinephrine is dispensable for the effects of chronic stress on cancer progression. Measured levels of circulating norepinephrine were sufficiently low that they were unlikely to influence beta(2-)adrenergic signaling, suggesting a possible role for norepinephrine release from sympathetic nerve terminals.
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