ArticleInternational journal of pancreatology : official journal of the International Association of Pancreatology2001
Expression of the IIIc variant of FGF receptor-1 confers mitogenic responsiveness to heparin and FGF-5 in TAKA-1 pancreatic ductal cells.
Article in International journal of pancreatology : official journal of the International Association of Pancreatology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 19 citations in OpenAlex.
- Splicing alterations in pancreatic ductal adenocarcinoma: a new molecular landscape with translational potential.Journal of experimental & clinical cancer research : CR · 2023Review
- Potential roles of FGF5 as a candidate therapeutic target in prostate cancer.American journal of clinical and experimental urology · 2023Review
- Deciphering role of FGFR signalling pathway in pancreatic cancer.Cell proliferation · 2019Review
- FGF5 promotes osteosarcoma cells proliferation via activating MAPK signaling pathway.Cancer management and research · 2019Article
- Inhibition of endogenous SPARC enhances pancreatic cancer cell growth: modulation by FGFR1-III isoform expression.British journal of cancer · 2010Article
- FGF5 as an oncogenic factor in human glioblastoma multiforme: autocrine and paracrine activities.Oncogene · 2008Article
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundFibroblast 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-1IIIc, implying a potential for autocrine growth modulation.
aimIn this study we investigated the importance of FGFR-1 IIIc expression for FGF-5 mitogenic signaling in a pancreatic ductal cell line.
methodsA cDNA encoding FGFR-1 IIIc was expressed in the well-differentiated TAKA-1 Syrian hamster pancreatic ductal cell line.
resultsTAKA-1 cells secrete FGF-5, but were found not to express FGFR-1 and to be unresponsive to exogenous FGF-5. In contrast, TAKA-1 clones expressing FGFR-1 IIIc were growth stimulated in the presence of FGF-5 and displayed enhanced mitogen-activated protein kinase (MAPK) activity in the presence of FGF-5. PD98059, an inhibitor of this pathway, inhibited FGF-5-induced growth in these clones.
conclusionOur data demonstrate that FGFR-1 IIIc can mediate FGF-5-induced mitogenesis via the MAPK pathway in pancreatic ductal cells, and suggest that expression of FGFR-1 IIIc in conjunction with FGF-5 may contribute to the pathobiology of human pancreatic cancer.
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