Journal
NATURE COMMUNICATIONS
Volume 7, Issue -, Pages -Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/ncomms10634
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Funding
- Australian National Health and Medical Research Council [1008865, 1053535]
- Australian Research Council [LE110100125]
- National Cancer Institute [CA160890]
- Australian and New Zealand College of Anaesthetists [N13/002]
- Monash Graduate Scholarship
- PhD scholarship from the Co-operative Research Centre for Cancer Therapeutics
- Swiss Cancer League
- Australian New Zealand College of Anaesthetists
- Australian National Health and Medical Research Council
- Early Career Fellowships from the National Breast Cancer Foundation
- Australian Research Council [LE110100125] Funding Source: Australian Research Council
- National Breast Cancer Foundation [NC-13-26] Funding Source: researchfish
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Chronic stress induces signalling from the sympathetic nervous system (SNS) and drives cancer progression, although the pathways of tumour cell dissemination are unclear. Here we show that chronic stress restructures lymphatic networks within and around tumours to provide pathways for tumour cell escape. We show that VEGFC derived from tumour cells is required for stress to induce lymphatic remodelling and that this depends on COX2 inflammatory signalling from macrophages. Pharmacological inhibition of SNS signalling blocks the effect of chronic stress on lymphatic remodelling in vivo and reduces lymphatic metastasis in preclinical cancer models and in patients with breast cancer. These findings reveal unanticipated communication between stress-induced neural signalling and inflammation, which regulates tumour lymphatic architecture and lymphogenous tumour cell dissemination. These findings suggest that limiting the effects of SNS signalling to prevent tumour cell dissemination through lymphatic routes may provide a strategy to improve cancer outcomes.
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