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  • Cao, RenhaiKarolinska Institutet (author)

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

  • Article/chapterEnglish2012

Publisher, publication year, extent ...

  • 2012-09-11
  • National Academy of Sciences,2012
  • printrdacarrier

Numbers

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

Supplementary language notes

  • Language:English
  • Summary in:English

Part of subdatabase

Classification

  • Subject category:ref swepub-contenttype
  • Subject category:art swepub-publicationtype

Notes

  • 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|
  • 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.

Subject headings and genre

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

Added entries (persons, corporate bodies, meetings, titles ...)

  • Ji, HongKarolinska Institutet (author)
  • Feng, NinghanDepartment of Microbiology, Tumor, and Cell Biology, Karolinska Institute, Stockholm, Sweden (author)
  • Zhang, YinKarolinska Institutet (author)
  • Yang, XiaojuanDepartment of Microbiology, Tumor, and Cell Biology, Karolinska Institute, Stockholm, Sweden (author)
  • Andersson, PatrikKarolinska Institutet (author)
  • Sun, YupingDepartment of Oncology, Jinan Central Hospital, Shandong University, Jinan, Shandong , People's Republic of China (author)
  • Tritsaris, KaterinaDepartment of Cellular and Molecular Medicine, Center for Healthy Aging Panum Institute, University of Copenhagen, Copenhagen, Denmark (author)
  • Jon Hansen, AnkerDepartment of Neuroscience and Pharmacology, Panum Institute, University of Copenhagen, Copenhagen, Denmark and Novo Nordisk A/S Måløv, Denmark (author)
  • Dissing, SteenDepartment of Cellular and Molecular Medicine, Center for Healthy Aging Panum Institute, University of Copenhagen, Copenhagen, Denmark (author)
  • Cao, YihaiKarolinska Institutet,Linköpings universitet,Avdelningen för kardiovaskulär medicin,Hälsouniversitetet,Department of Microbiology, Tumor, and Cell Biology, Karolinska Institute, Sweden(Swepub:liu)yihca64 (author)
  • Karolinska InstitutetDepartment of Microbiology, Tumor, and Cell Biology, Karolinska Institute, Stockholm, Sweden (creator_code:org_t)

Related titles

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

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