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  3. Receptor FGFRL1 acts as a tumor suppressor in nude mice when overexpressed in HEK 293 Tet-On cells.
 

Receptor FGFRL1 acts as a tumor suppressor in nude mice when overexpressed in HEK 293 Tet-On cells.

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BORIS DOI
10.7892/boris.95677
Publisher DOI
10.3892/ol.2016.5245
PubMed ID
28101211
Description
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.
Date of Publication
2016-12
Publication Type
Article
Subject(s)
600 Technology > 610 Medicine & health
Keyword(s)
FGF
•
FGFR
•
FGFRL1
•
cell adhesion
•
tumor suppressor
Language(s)
en
Contributor(s)
Zhuang, Lei
Universitätsklinik für Rheumatologie, Immunologie und Allergologie
Steinberg, Florian
Trueb, Beatorcid-logo
Universitätsklinik für Rheumatologie, Immunologie und Allergologie, Teilklinik Rheumatologie
Additional Credits
Universitätsklinik für Rheumatologie, Immunologie und Allergologie
Universitätsklinik für Rheumatologie, Immunologie und Allergologie, Teilklinik Rheumatologie
Series
Oncology letters
Publisher
Spandidos Publications
ISSN
1792-1074
Access(Rights)
open.access
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