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Sökning: onr:"swepub:oai:DiVA.org:liu-85089" > Collaborative inter...

Collaborative interplay between FGF-2 and VEGF-C promotes lymphangiogenesis and metastasis

Cao, Renhai (författare)
Karolinska Institutet
Ji, Hong (författare)
Karolinska Institutet
Feng, Ninghan (författare)
Department of Microbiology, Tumor, and Cell Biology, Karolinska Institute, Stockholm, Sweden
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Zhang, Yin (författare)
Karolinska Institutet
Yang, Xiaojuan (författare)
Department of Microbiology, Tumor, and Cell Biology, Karolinska Institute, Stockholm, Sweden
Andersson, Patrik (författare)
Karolinska Institutet
Sun, Yuping (författare)
Department of Oncology, Jinan Central Hospital, Shandong University, Jinan, Shandong , People's Republic of China
Tritsaris, Katerina (författare)
Department of Cellular and Molecular Medicine, Center for Healthy Aging Panum Institute, University of Copenhagen, Copenhagen, Denmark
Jon Hansen, Anker (författare)
Department of Neuroscience and Pharmacology, Panum Institute, University of Copenhagen, Copenhagen, Denmark and Novo Nordisk A/S Måløv, Denmark
Dissing, Steen (författare)
Department of Cellular and Molecular Medicine, Center for Healthy Aging Panum Institute, University of Copenhagen, Copenhagen, Denmark
Cao, Yihai (författare)
Karolinska Institutet,Linköpings universitet,Avdelningen för kardiovaskulär medicin,Hälsouniversitetet,Department of Microbiology, Tumor, and Cell Biology, Karolinska Institute, Sweden
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 (creator_code:org_t)
2012-09-11
2012
Engelska.
Ingår i: Proceedings of the National Academy of Sciences of the United States of America. - : National Academy of Sciences. - 0027-8424 .- 1091-6490. ; 109:39, s. 15894-15899
Relaterad länk:
https://www.pnas.org...
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https://urn.kb.se/re...
https://doi.org/10.1...
http://kipublication...
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  • Tidskriftsartikel (refereegranskat)
Abstract Ämnesord
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  • 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.

Nyckelord

neovascularization
growth factors
signaling interplay
cancer spread
antiangiogenic therapy
SOCIAL SCIENCES
SAMHÄLLSVETENSKAP

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