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Receptor FGFRL1 acts as a tumor suppressor in nude mice when overexpressed in HEK 293 Tet-On cells.
Zhuang, Lei; Steinberg, Florian; Trueb, Beat.
Afiliação
  • Zhuang L; Department of Clinical Research, University of Bern, CH-3008 Bern, Switzerland.
  • Steinberg F; Department of Clinical Research, University of Bern, CH-3008 Bern, Switzerland; Center for Biological Systems Analysis, University of Freiburg, D-79104 Freiburg, Germany.
  • Trueb B; Department of Clinical Research, University of Bern, CH-3008 Bern, Switzerland; Department of Rheumatology, University Hospital, CH-3010 Bern, Switzerland.
Oncol Lett ; 12(6): 4524-4530, 2016 Dec.
Article em En | MEDLINE | ID: mdl-28101211
Fibroblast growth factor receptor-like 1 (FGFRL1) is a transmembrane receptor that interacts with heparin and FGF ligands. In contrast to the classical FGF receptors, FGFR1 to FGFR4, it does not appear to affect cell growth and proliferation. In the present study, an inducible gene expression system was utilized in combination with a xenograft tumor model to investigate the effects of FGFRL1 on cell adhesion and tumor formation. It was determined that recombinant FGFRL1 promotes the adhesion of HEK 293 Tet-On® cells in vitro. Moreover, when such cells are induced to express FGFRL1ΔC they aggregate into huge clusters. If injected into nude mice, the cells form large tumors. Notably, this tumor growth is completely inhibited when the expression of FGFRL1 is induced. The forced expression of FGFRL1 in the tumor tissue may restore contact inhibition, thereby preventing growth of the cells in nude mice. The results of the present study demonstrate that FGFRL1 acts as a tumor suppressor similar to numerous other cell adhesion proteins. It is therefore likely that FGFRL1 functions as a regular cell-cell adhesion protein.
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Tipo de estudo: Prognostic_studies Idioma: En Ano de publicação: 2016 Tipo de documento: Article

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Tipo de estudo: Prognostic_studies Idioma: En Ano de publicação: 2016 Tipo de documento: Article