Expression of the IIIc variant of FGF receptor-1 confers mitogenic responsiveness to heparin and FGF-5 in TAKA-1 pancreatic ductal cells

@article{Kornmann2001ExpressionOT,
  title={Expression of the IIIc variant of FGF receptor-1 confers mitogenic responsiveness to heparin and FGF-5 in TAKA-1 pancreatic ductal cells},
  author={Marko Kornmann and Martha E. Lopez and Hans G. Beger and Murray Korc},
  journal={International Journal of Pancreatology},
  year={2001},
  volume={29},
  pages={85-92}
}
SummaryBackground. Fibroblast growth factors (FGFs) contribute to angiogenesis and mitogenesis by binding to tyrosine kinase receptors termed FGF receptors (FGFRs). FGF-5 is a secreted FGF that is believed to preferentially act via the IIIc splice variant of FGFR-1. Human pancreatic ductal carcinoma cells express FGF-5 and FGFR-1 IIIc, implying a potential for autocrine growth modulation.Aim. In this study we investigated the importance of FGFR-1 IIIc expression for FGF-5 mitogenic signaling in… 
IIIc isoform of fibroblast growth factor receptor 1 is overexpressed in human pancreatic cancer and enhances tumorigenicity of hamster ductal cells.
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The data indicate that FGFR-1 IIIc is expressed in human pancreatic cancer cells, promotes mitogenic signaling via the FRS2-MAPK pathway, and has the potential to enhance pancreatic ductal cell transformation.
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The results demonstrate that the human FGFR-1 IIIb variant is a functional FGFR expressed in the pancreas that can alter pancreatic functions that regulate proliferation, adhesion, and movement.
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TLDR
The results show that FGFR1-IIIb is a functional FGFR that inhibits the transformed phenotype of human pancreatic cancer cells.
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Fibroblast growth factor receptor 1 (FGFR1) isoform IIIc enhances and FGFR1-IIIb inhibits pancreatic cancer cell growth for the first time and is differentially regulated by growth factors and cyclin D1.
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It is demonstrated for the first time that FGF5 contributes to the malignant progression of human astrocytic brain tumours by both autocrine and paracrine effects.
Gastrointestinal , Hepatobiliary , and Pancreatic Pathology Enhanced Expression of Fibroblast Growth Factor Receptor 2 IIIc Promotes Human Pancreatic Cancer Cell Proliferation
In pancreatic ductal adenocarcinoma (PDAC), the fibroblast growth factor receptor 1 (FGFR-1) IIIb isoform correlates with the inhibition of cancer cell proliferation, migration, and invasion, whereas
Nuclear translocation of FGFR 1 and FGF 2 in pancreatic stellate cells facilitates pancreatic cancer cell invasion
TLDR
In vitro inhibiting FGFR1 and FGF2 in PSCs, using RNAi or chemical inhibition, resulted in significantly reduced cell proliferation, which was not seen in cancer cells, suggesting a novel therapeutic approach, where preventing nuclear FGF/FGFR mediated proliferation and invasion in P SCs leads to disruption of the tumour microenvironment, preventing pancreatic cancer cell invasion.
Nuclear translocation of FGFR1 and FGF2 in pancreatic stellate cells facilitates pancreatic cancer cell invasion
TLDR
In vitro inhibiting FGFR1 and FGF2 in PSCs, using RNAi or chemical inhibition, resulted in significantly reduced cell proliferation, which was not seen in cancer cells, suggesting a novel therapeutic approach, where preventing nuclear FGF/FGFR mediated proliferation and invasion in P SCs leads to disruption of the tumour microenvironment, preventing pancreatic cancer cell invasion.
FGF5 promotes osteosarcoma cells proliferation via activating MAPK signaling pathway
TLDR
It is demonstrated for the first time that FGF5 was overexpressed in OS cell lines and clinical tissue samples and promotes OS cell proliferation by activating MAPK signaling pathway, which indicated that F GF5 was a potential therapeutic target for OS.
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