Journal
ONCOTARGET
Volume 3, Issue 8, Pages 893-906Publisher
IMPACT JOURNALS LLC
DOI: 10.18632/oncotarget.593
Keywords
Cancer; Metastasis; VEGF-D; Lymphatics; Lymphangiogenesis; Angiogenesis; Prostaglandin; PGDH; COX-1; COX-2; NSAID; Aspirin
Categories
Funding
- National Health and Medical Research Council of Australia
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Substantial evidence supports important independent roles for lymphangiogenic growth factor signaling and prostaglandins in the metastatic spread of cancer. The significance of the lymphangiogenic growth factors, vascular endothelial growth factor (VEGF)-C and VEGF-D, is well established in animal models of metastasis, and a strong correlation exits between an increase in expression of VEGF-C and VEGF-D, and metastatic spread in various solid human cancers. Similarly, key enzymes that control the production of prostaglandins, cyclooxygenases (COX-1 and COX-2, prototypic targets of Non-steroidal anti-inflammatory drugs (NSAIDs)), are frequently over-expressed or de-regulated in the progression of cancer. Recent data have suggested an intersection of lymphangiogenic growth factor signaling and the prostaglandin pathways in the control of metastatic spread via the lymphatic vasculature. Furthermore, this correlates with current clinical data showing that some NSAIDs enhance the survival of cancer patients through reducing metastasis. Here, we discuss the potential biochemical and cellular basis for such anti-cancer effects of NSAIDs through the prostaglandin and VEGF signaling pathways.
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