Journal
CANCER CELL
Volume 21, Issue 2, Pages 181-195Publisher
CELL PRESS
DOI: 10.1016/j.ccr.2011.12.026
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Funding
- National Health and Medical Research Council of Australia (NHMRC)
- Victorian Government, Australia
- NHMRC [1008865]
- Pfizer Australia
- Raelene Boyle Sporting Chance Foundation
- Royal Australasian College of Surgeons (RAGS) Foundation
- National Breast Cancer Foundation
- University of Melbourne, Australia
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Lymphatic metastasis is facilitated by lymphangiogenic growth factors VEGF-C and VEGF-D that are secreted by some primary tumors. We identified regulation of PGDH, the key enzyme in prostaglandin catabolism, in endothelial cells of collecting lymphatics, as a key molecular change during VEGF-D-driven tumor spread. The VEGF-D-dependent regulation of the prostaglandin pathway was supported by the finding that collecting lymphatic vessel dilation and subsequent metastasis were affected by nonsteroidal anti-inflammatory drugs (NSAIDs), known inhibitors of prostaglandin synthesis. Our data suggest a control point for cancer metastasis within the collecting lymphatic endothelium, which links VEGF-DNEGFR-2/VEGFR-3 and the prostaglandin pathways. Collecting lymphatics therefore play an active and important role in metastasis and may provide a therapeutic target to restrict tumor spread.
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