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

  • 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

Förlag, utgivningsår, omfång ...

  • National Academy of Sciences,2012
  • printrdacarrier

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

Kompletterande språkuppgifter

  • Språk:engelska
  • Sammanfattning på:engelska

Ingår i deldatabas

Klassifikation

  • Ämneskategori:ref swepub-contenttype
  • 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

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