Browse by author
Lookup NU author(s): Dr Piyush Mehta, Professor Craig Robson, Professor David Neal, Professor Hing Leung
Full text for this publication is not currently held within this repository. Alternative links are provided below where available.
FGF7/Keratinocyte growth factor (KGF) regulates the differentiation and development of the prostate epithelium, while over-expression of FGF8 and FGF1 are implicated in carcinogenesis of the prostate. We tested the hypothesis that different members of the FGF family function through different signalling molecules. In prostate DU145 cells, both FGF1 and FGF2 activated ERK1/2 potently and p38 moderately. KGF was however most efficient in inducing p38 activities but had no effect on ERK1/2 function. JNK and STAT activities were not induced by FGFs in prostate cells. In vitro expression of the transcription factors Elk-1 and MEF2A (substrates for ERK1/2 and p38, respectively) for functional quantification, confirmed the pattern of FGF-induced MAPK activations in COS-7 cells. Furthermore, KGF was more efficient than FGF1 and FGF2 in inducing actin stress fibres, and the specific p38 inhibitor SB202190 completely abolished this in a dose-dependent manner. The MEK1/2 inhibitor, U0126, had no effect on FGF-induced stress fibre formation. This study demonstrates the selective activation of MAPK family members by FGFs resulting in activation of transcription factors and stress fibre formation. As multiple FGFs are overexpressed in human prostate cancer, characterization of the distinct signalling pathway by FGFs may reveal new specific targets for therapy.
Author(s): Mehta, P. B., Robson, C. N., Neal, D. E., Leung, H. Y.
Publication type: Article
Publication status: Published
Journal: Oncogene
Year: 2001
Volume: 20
Issue: 38
Pages: 5359-5365
Print publication date: 30/08/2001
ISSN (print): 0950-9232
ISSN (electronic): 1476-5594
URL: http://dx.doi.org/10.1038/sj.onc.1204688
DOI: 10.1038/sj.onc.1204688
PubMed id: 11536048
Altmetrics provided by Altmetric
