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Inhibition of both focal adhesion kinase and fibroblast growth factor receptor 2 pathways induces anti-tumor and anti-angiogenic activities

Authors
  • Dao, Pascal
  • Jarray, Rafika
  • Smith, Nikaia
  • Lepelletier, Yves
  • Coq, Johanne Le
  • Lietha, Daniel
  • Hadj-Slimane, Réda
  • Herbeuval, Jean-Philippe
  • Garbay, Christiane
  • Raynaud, Françoise
  • Chen, Huixiong1, 2, 3, 4, 5, 6, 7, 4, 5, 8, 9, 10, 11, 12, 13
  • 1 CNRS, UMR8601
  • 2 Laboratoire de Chimie et Biochimie Pharmacologiques et Toxicologiques
  • 3 CBNIT
  • 4 Université Paris Descartes
  • 5 PRES Sorbonne Paris Cité
  • 6 UFR Biomédicale
  • 7 UMR CNRS 8147
  • 8 Hôpital Necker
  • 9 Structural Biology and Biocomputing Programme
  • 10 Spanish National Cancer Research Centre (CNIO)
  • 11 Visiotact Pharma
  • 12 School of Chemical Engineering and Light Industry
  • 13 Guangdong University of Technology
Type
Published Article
Journal
Cancer Letters
Publisher
Elsevier
Publication Date
Jan 01, 2014
Accepted Date
Mar 07, 2014
Identifiers
DOI: 10.1016/j.canlet.2014.03.007
Source
Elsevier
Keywords
License
Unknown

Abstract

FAK and FGFR2 signaling pathways play important roles in cancer development, progression and tumor angiogenesis. PHM16 is a novel ATP competitive inhibitor of FAK and FGFR2. To evaluate the therapeutic efficacy of this agent, we examined its anti-angiogenic effect in HUVEC and its anti-tumor effect in different cancer cell lines. We showed PHM16 inhibited endothelial cell viability, adherence and tube formation along with the added ability to induce endothelial cell apoptosis. This compound significantly delayed tumor cell growth. Together, these data showed that inhibition of both FAK and FGFR2 signaling pathways can enhance anti-tumor and anti-angiogenic activities.

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