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(American Journal of Pathology. 2001;159:893-903.)
© 2001 American Society for Investigative Pathology

Regular Articles

Concurrent Induction of Lymphangiogenesis, Angiogenesis, and Macrophage Recruitment by Vascular Endothelial Growth Factor-C in Melanoma

Mihaela Skobe*, Leena M. Hamberg{dagger}, Thomas Hawighorst*, Michael Schirner{ddagger}, Gerald L. Wolf{dagger}, Kari Alitalo§ and Michael Detmar*

From the Department of Dermatology,*
Cutaneous Biology Research Center, and the Center for Imaging and Pharmaceutical Research,{dagger}
Massachusetts General Hospital and Harvard Medical School, Charlestown, Massachusetts; Schering AG,{ddagger}
Berlin, Germany; and the Haartman Institute,§
University of Helsinki, Helsinki, Finland

Interactions of tumor cells with lymphatic vessels are of paramount importance for tumor progression, however, the underlying molecular mechanisms are poorly understood. Whereas enlarged lymphatic vessels are frequently observed at the periphery of malignant melanomas, it has remained unclear whether intratumoral lymphangiogenesis occurs within these tumors. Here, we demonstrate the presence of intratumoral lymphatics and enlargement of lymphatic vessels at the tumor periphery in vascular endothelial growth factor (VEGF)-C-overexpressing human melanomas transplanted onto nude mice. VEGF-C expression also resulted in enhanced tumor angiogenesis, indicating a coordinated regulation of lymphangiogenesis and angiogenesis in melanoma progression. The specific biological effects of VEGF-C were critically dependent on its proteolytic processing in vivo. Furthermore, VEGF-C induced chemotaxis of macrophages in vitro and in vivo, revealing a potential function of VEGF-C as an immunomodulator. Taken together, our results identify VEGF-C as multifunctional factor involved in regulating tumor lymphangiogenesis, angiogenesis, and immune response.




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