Role of fibroblast growth factor 8 in growth and progression of hormonal cancer

Mattila, Mirjami; Härkönen, Pirkko

doi:10.1016/j.cytogfr.2007.04.010

Cited by 71 publications

(80 citation statements)

References 100 publications

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“…The roles of FGF8f signaling and MAPK pathways in osteoblastic differentiation FGF8 is one of most extensively studied FGF family member that modulates a balance between proliferation and differentiation (Mattila and Harkonen, 2007). Although many studies have shown that FGF8 regulates osteoblast development and bone formation (Ornitz and Marie, 2002;Jackson et al, 2006), the distinct physiological functions of different FGF8 isoforms in such regulations are unknown.…”

Section: Ra-mediated Rara Hypophosphorylation Induces Fgf8f Expressionmentioning

confidence: 99%

Retinoid-suppressed phosphorylation of RARα mediates the differentiation pathway of osteosarcoma cells

et al. 2010

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Section: Ra-mediated Rara Hypophosphorylation Induces Fgf8f Expressionmentioning

confidence: 99%

Retinoid-suppressed phosphorylation of RARα mediates the differentiation pathway of osteosarcoma cells

et al. 2010

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“…Experimental data suggests that FGF-8 is associated with development and progression of breast cancer (Mattila and Harkonen, 2007). Mice over expressing FGF-8 have provided evidence that FGF-8 contributes to mammary gland tumorigenesis (Daphna-Iken et al, 1998) and over expression of FGF-8 in murine S115 cells and human MCF-7 cells leads to increased tumor growth and angiogenesis in nude mice (Mattila et al, 2001;Ruohola et al, 2001).…”

Section: Introductionmentioning

confidence: 99%

Identification of fibroblast growth factor-8b target genes associated with early and late cell cycle events in breast cancer cells

Nilsson

Brokken

Narvi

et al. 2012

Molecular and Cellular Endocrinology

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(2012). Identification of fibroblast growth factor-8b target genes associated with early and late cell cycle events in breast cancer cells. Molecular and Cellular Endocrinology, 358(1), 104-115. DOI: 10.1016/j.mce.2012.03.009 General rights Copyright and moral rights for the publications made accessible in the public portal are retained by the authors and/or other copyright owners and it is a condition of accessing publications that users recognise and abide by the legal requirements associated with these rights.• Users may download and print one copy of any publication from the public portal for the purpose of private study or research.• You may not further distribute the material or use it for any profit-making activity or commercial gain • You may freely distribute the URL identifying the publication in the public portal

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“…Experimental and clinical data point to a nonredundant autocrine/paracrine role of FGF8 in the growth of epithelial/stromal cells in steroid hormone-regulated tumors (2,3), the FGF8 gene containing a functional androgen-response element responsible for its transcriptional activation by steroid-receptor signaling (4). Various alternatively spliced FGF8 isoforms are generated in mice and humans.…”

Section: Introductionmentioning

confidence: 99%

Long Pentraxin-3 Inhibits FGF8b-Dependent Angiogenesis and Growth of Steroid Hormone–Regulated Tumors

Leali

Alessi

Coltrini

et al. 2011

Molecular Cancer Therapeutics

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Fibroblast growth factor-8b (FGF8b) exerts nonredundant autocrine/paracrine functions in steroid hormone-regulated tumors. Previous observations had shown that the soluble pattern recognition receptor long pentraxin-3 (PTX3) is a natural selective antagonist for a restricted number of FGF family members, inhibiting FGF2 but not FGF1 and FGF4 activity. Here, we assessed the capacity of PTX3 to antagonize FGF8b and to inhibit the vascularization and growth of steroid hormone-regulated tumors. Surface plasmon resonance analysis shows that PTX3 binds FGF8b with high affinity (K d ¼ 30-90 nmol/L). As a consequence, PTX3 prevents the binding of FGF8b to its receptors, inhibits FGF8b-driven ERK1/2 activation, cell proliferation, and chemotaxis in endothelial cells, and suppresses FGF8b-induced neovascularization in vivo. Also, PTX3 inhibits dihydrotestosterone (DHT)-and FGF8b-driven proliferation of androgen-regulated Shionogi 115 (S115) mouse breast tumor cells. Furthermore, DHT-treated, PTX3 overexpressing hPTX3_S115 cell transfectants show a reduced proliferation rate in vitro and a limited angiogenic activity in the chick embryo chorioallantoic membrane and murine s.c. Matrigel plug assays. Accordingly, hPTX3_S115 cells show a dramatic decrease of their tumorigenic activity when grafted in immunodeficient male mice. These results identify PTX3 as a novel FGF8b antagonist endowed with antiangiogenic and antineoplastic activity with possible implications for the therapy of hormonal tumors. Mol Cancer Ther; 10(9); 1600-10. Ó2011 AACR.

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Role of fibroblast growth factor 8 in growth and progression of hormonal cancer

Cited by 71 publications

References 100 publications

Retinoid-suppressed phosphorylation of RARα mediates the differentiation pathway of osteosarcoma cells

Retinoid-suppressed phosphorylation of RARα mediates the differentiation pathway of osteosarcoma cells

Identification of fibroblast growth factor-8b target genes associated with early and late cell cycle events in breast cancer cells

Long Pentraxin-3 Inhibits FGF8b-Dependent Angiogenesis and Growth of Steroid Hormone–Regulated Tumors

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