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

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Cao, RenhaiDepartment of Microbiology, Tumor, and Cell Biology, Karolinska Institute, Stockholm, Sweden (författare)

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

Artikel/kapitelEngelska2012

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National Academy of Sciences,2012
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Nummerbeteckningar

LIBRIS-ID:oai:DiVA.org:liu-85089
urn:nbn:se:liu:diva-85089urn
https://doi.org/10.1073/pnas.1208324109DOI
http://kipublications.ki.se/Default.aspx?queryparsed=id:125387598URI

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Språk:engelska
Sammanfattning på:engelska

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Ämneskategori:art swepub-publicationtype

Anmärkningar

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|
gratis
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.

Ämnesord och genrebeteckningar

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

Biuppslag (personer, institutioner, konferenser, titlar ...)

Ji, HongDepartment of Microbiology, Tumor, and Cell Biology, Karolinska Institute, Stockholm, Sweden (författare)
Feng, NinghanDepartment of Microbiology, Tumor, and Cell Biology, Karolinska Institute, Stockholm, Sweden (författare)
Zhang, YinDepartment of Microbiology, Tumor, and Cell Biology, Karolinska Institute, Stockholm, Sweden (författare)
Yang, XiaojuanDepartment of Microbiology, Tumor, and Cell Biology, Karolinska Institute, Stockholm, Sweden (författare)
Andersson, PatrikDepartment of Microbiology, Tumor, and Cell Biology, Karolinska Institute, Stockholm, Sweden (författare)
Sun, YupingDepartment of Oncology, Jinan Central Hospital, Shandong University, Jinan, Shandong , People's Republic of China (författare)
Tritsaris, KaterinaDepartment of Cellular and Molecular Medicine, Center for Healthy Aging Panum Institute, University of Copenhagen, Copenhagen, Denmark (författare)
Jon Hansen, AnkerDepartment of Neuroscience and Pharmacology, Panum Institute, University of Copenhagen, Copenhagen, Denmark and Novo Nordisk A/S Måløv, Denmark (författare)
Dissing, SteenDepartment of Cellular and Molecular Medicine, Center for Healthy Aging Panum Institute, University of Copenhagen, Copenhagen, Denmark (författare)
Cao, YihaiLinköpings universitet,Avdelningen för kardiovaskulär medicin,Hälsouniversitetet,Department of Microbiology, Tumor, and Cell Biology, Karolinska Institute, Sweden(Swepub:liu)yihca64 (författare)
Feng, NH (författare)
Hansen, AJ (författare)
Ji, HKarolinska Institutet(Swepub:ki)03c60178ea0bfafb3180b00e64adac5f (författare)
Dissing, S (författare)
Cao, YHKarolinska Institutet(Swepub:ki)58da69c79b670cbdce9774f91e5c302d (författare)
Zhang, YKarolinska Institutet(Swepub:ki)847b9fdef4105b9d4e0ac89913751c81 (författare)
Yang, XJ (författare)
Cao, RHKarolinska Institutet(Swepub:ki)887b231da0c4c5844bad37d158d7b1b7 (författare)
Andersson, PKarolinska Institutet(Swepub:ki)a03738568206e93f65e76e917477afec (författare)
Tritsaris, K (författare)
Sun, YP (författare)
Department of Microbiology, Tumor, and Cell Biology, Karolinska Institute, Stockholm, SwedenDepartment of Oncology, Jinan Central Hospital, Shandong University, Jinan, Shandong , People's Republic of China (creator_code:org_t)

Sammanhörande titlar

Ingår i:Proceedings of the National Academy of Sciences of the United States of America: National Academy of Sciences109:39, s. 15894-158990027-84241091-6490