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Collaborative interplay between FGF-2 and VEGF-C promotes lymphangiogenesis and metastasis
Department of Microbiology, Tumor, and Cell Biology, Karolinska Institute, Stockholm, Sweden.
Department of Microbiology, Tumor, and Cell Biology, Karolinska Institute, Stockholm, Sweden.
Department of Microbiology, Tumor, and Cell Biology, Karolinska Institute, Stockholm, Sweden.
Department of Microbiology, Tumor, and Cell Biology, Karolinska Institute, Stockholm, Sweden.
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2012 (Engelska)Ingår i: Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, E-ISSN 1091-6490, Vol. 109, nr 39, s. 15894-15899Artikel i tidskrift (Refereegranskat) Published
Abstract [en]

Interplay between various lymphangiogenic factors in promoting lymphangiogenesis and lymphatic metastasis remains poorly understood. Here we show that FGF-2 and VEGF-C, two lymphangiogenic factors, collaboratively promote angiogenesis and lymphangiogenesis in the tumor microenvironment, leading to widespread pulmonary and lymph-node metastases. Coimplantation of dual factors in the mouse cornea resulted in additive angiogenesis and lymphangiogenesis. At the molecular level, we showed that FGFR-1 expressed in lymphatic endothelial cells is a crucial receptor that mediates the FGF-2-induced lymphangiogenesis. Intriguingly, the VEGFR-3-mediated signaling was required for the lymphatic tip cell formation in both FGF-2- and VEGF-C-induced lymphangiogenesis. Consequently, a VEGFR-3-specific neutralizing antibody markedly inhibited FGF-2-induced lymphangiogenesis. Thus, the VEGFR-3-induced lymphatic endothelial cell tip cell formation is a prerequisite for FGF-2-stimulated lymphangiogenesis. In the tumor microenvironment, the reciprocal interplay between FGF-2 and VEGF-C collaboratively stimulated tumor growth, angiogenesis, intratumoral lymphangiogenesis, and metastasis. Thus, intervention and targeting of the FGF-2- and VEGF-C-induced angiogenic and lymphangiogenic synergism could be potentially important approaches for cancer therapy and prevention of metastasis.

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National Academy of Sciences , 2012. Vol. 109, nr 39, s. 15894-15899
Nyckelord [en]
neovascularization, growth factors, signaling interplay, cancer spread, antiangiogenic therapy
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URN: urn:nbn:se:liu:diva-85089DOI: 10.1073/pnas.1208324109ISI: 000309604500074OAI: oai:DiVA.org:liu-85089DiVA, id: diva2:564623
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Funding Agencies|Swedish Research Council||Swedish Cancer Foundation||Karolinska Institute Foundation||Karolinska Institute distinguished professor award||Torsten Soderbergs Foundation||ImClone Systems/EliLilly||European Union Integrated Project of Metoxia|222741|Nordea Foundation||European Research Council advanced Grant ANGIOFAT|250021|

Tillgänglig från: 2012-11-02 Skapad: 2012-11-02 Senast uppdaterad: 2017-12-07Bibliografiskt granskad

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