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Open AccessJournal ArticleDOI

Fibroblast growth factors, their receptors and signaling.

Ciaran Powers, +2 more
- 01 Sep 2000 - 
- Vol. 7, Iss: 3, pp 165-197
TLDR
FGF signaling also appears to play a role in tumor growth and angiogenesis, and autocrine FGF signaling may be particularly important in the progression of steroid hormone-dependent cancers to a hormone-independent state.
Abstract
Fibroblast growth factors (FGFs) are small polypeptide growth factors, all of whom share in common certain structural characteristics, and most of whom bind heparin avidly. Many FGFs contain signal peptides for secretion and are secreted into the extracellular environment, where theycan bind to the heparan-like glycosaminoglycans (HLGAGs) of the extracellular matrix (ECM). From this reservoir, FGFs mayact directlyon target cells, or theycan be released through digestion of the ECM or the activityof a carrier protein, a secreted FGF binding protein. FGFs bind specific receptor tyrosine kinases in the context of HLGAGs and this binding induces receptor dimerization and activation, ultimatelyresulting in the activation of various signal transduction cascades. Some FGFs are potent angiogenic factors and most playimportant roles in embry onic development and wound healing. FGF signaling also appears to playa role in tumor growth and angiogenesis, and autocrine FGF signaling maybe particularlyimportant in the progression of steroid hormone-dependent cancers to a hormone-independent state.

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Journal ArticleDOI

Epithelial Fibroblast Growth Factor Receptor 1 Regulates Enamel Formation

TL;DR: There is a cell-autonomous requirement for FGF signaling in the dental epithelium during enamel formation, as loss of Fgfr1 affects ameloblast organization at the enamel-secretory stage and, hence, the formation of enamel.
Journal ArticleDOI

FGF-8b induces growth and rich vascularization in an orthotopic PC-3 model of prostate cancer.

TL;DR: It is demonstrated that FGF‐8b increases the growth and angiogenesis of orthotopic prostate tumors and the associated gene expression signature suggests potential mediators for FGF•8b actions on prostate cancer progression and metastasis.
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The Human Sef-a Isoform Utilizes Different Mechanisms to Regulate Receptor Tyrosine Kinase Signaling Pathways and Subsequent Cell Fate

TL;DR: It is shown that hSef-a is a multifunctional negative modulator of RTK signaling and clearly demonstrate that hEstate-a can inhibit the activation of MAPK, although in a cell type-specific manner.
Journal ArticleDOI

Anti-tumor effects of fibroblast growth factor-binding protein (FGF-BP) knockdown in colon carcinoma.

TL;DR: It is shown that the systemic treatment of mice leads to the inhibition of tumor growth based on FGF-BP knockdown, and represents a promising therapeutic target for RNAi-based knockdown approaches.
Journal ArticleDOI

Modulation of energy balance by fibroblast growth factor 21.

TL;DR: Clinical evaluation of therapeutic action of exogenous FGF21 administration is warranted, particularly to treat diabetes and obesity, as Interestingly, energy expenditure and weight loss is induced by FGF 21.
References
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Journal ArticleDOI

Cell surface, heparin-like molecules are required for binding of basic fibroblast growth factor to its high affinity receptor.

TL;DR: It is demonstrated that free heparin and heparan sulfate can reconstitute a low affinity receptor that is, in turn, required for the high affinity binding of bFGF.
Journal ArticleDOI

Protein modules and signalling networks

TL;DR: This work highlights conserved protein domains that act as key regulatory participants in many of these different signalling pathways in multicellular organisms.
Journal ArticleDOI

Thalidomide is an inhibitor of angiogenesis.

TL;DR: Electron microscopic examination of the corneal neovascularization of thalidomide-treated rabbits revealed specific ultrastructural changes similar to those seen in the deformed limb bud vasculature of Thalidomid-treated embryos.
Journal ArticleDOI

Receptor specificity of the fibroblast growth factor family.

TL;DR: It is demonstrated that FGF 1 is the only FGF that can activate all FGF receptor splice variants and the relative activity of all the other members of the FGF family is determined.
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