Fibroblast growth factors in cancer: therapeutic possibilities

Jeffers, Michael; LaRochelle, William J.; Lichenstein, Henri S.

doi:10.1517/14728222.6.4.469

Cited by 55 publications

(38 citation statements)

References 102 publications

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“…Indeed, FGF2 upregulation in melanoma cells (12) has been linked to melanoma progression (13) and is accompanied by the expression of FGFRs that trigger an autocrine loop of stimulation critical for the survival and growth of melanoma cells. In parallel, FGF2 induces a proangiogenic response by acting on FGFR1-expressing endothelial cells via a paracrine mechanism of action (8), thus supporting tumor growth and hematogenous dissemination of metastatic cells.…”

Section: Discussionmentioning

confidence: 99%

“…The FGF gene family encompasses 22 members (10) that exert their activity by binding to tyrosine kinase FGF receptors (FGFR) expressed by 4 distinct FGFR1 to FGFR4 genes (11). FGF2 expression is an important feature of melanoma cells (12) and it has been linked to tumor progression in melanoma and various other malignancies (13). FGF2 production is paralleled by the expression of FGFRs that trigger an autocrine loop of stimulation critical for the survival and growth of melanoma cells (12,14).…”

Section: Introductionmentioning

confidence: 99%

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Long Pentraxin-3 Inhibits Epithelial–Mesenchymal Transition in Melanoma Cells

Ronca

Salle

Giacomini

et al. 2013

Molecular Cancer Therapeutics

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During melanoma progression, malignant melanocytes are reprogrammed into mesenchymal-like cells through to an epithelial-mesenchymal transition (EMT) process associated with the acquisition of an invasive, prometastatic phenotype. The fibroblast growth factor-2 (FGF2)/FGF receptor (FGFR) system plays a pivotal role in melanoma, leading to autocrine/paracrine induction of tumor cell proliferation and angiogenesis. Long pentraxin-3 (PTX3) interacts with FGF2, and other FGF family members, inhibiting FGF-dependent neovascularization and tumor growth. Here, PTX3 protein and the PTX3-derived acetylated pentapeptide Ac-ARPCA-NH 2 inhibit FGF2-driven proliferation and downstream FGFR signaling in murine melanoma B16-F10 cells. Moreover, human PTX3-overexpressing hPTX_B16-F10 cells are characterized by the reversed transition from a mesenchymal to an epithelial-like appearance, inhibition of cell proliferation, loss of clonogenic potential, reduced motility and invasive capacity, downregulation of various mesenchymal markers, and upregulation of the epithelial marker E-cadherin. Accordingly, PTX3 affects cell proliferation and EMT transition in human A375 and A2058 melanoma cells. Also, hPTX_B16-F10 cells showed a reduced tumorigenic and metastatic activity in syngeneic C57BL/6 mice. In conclusion, PTX3 inhibits FGF/FGFR-driven EMT in melanoma cells, hampering their tumorigenic and metastatic potential. These data represent the first experimental evidence about a nonredundant role of the FGF/FGFR system in the modulation of the EMT process in melanoma and indicate that PTX3 or its derivatives may represent the basis for the design of novel therapeutic approaches in FGF/FGFRdependent tumors, including melanoma. Mol Cancer Ther; 12(12); 2760-71. Ó2013 AACR.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Long Pentraxin-3 Inhibits Epithelial–Mesenchymal Transition in Melanoma Cells

Ronca

Salle

Giacomini

et al. 2013

Molecular Cancer Therapeutics

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“…Accumulating evidence has shown that members of the FGF family together with their transmembrane tyrosine kinase receptors (FGFR) may act as autocrine as well as paracrine (angiogenic) growth factors in many, if not all, solid tumors (26). FGFs act as mitogens and some members induce cell migration, angiogenesis, neurite outgrowth and cell survival (27).…”

Section: Fgfr1 Gene Status ------------------------------------------mentioning

confidence: 99%

Increased FGFR1 copy number in lung squamous cell carcinomas

et al. 2011

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Abstract. The basic fibroblast growth factor (bFGF), via activation of its receptor, FGFR1, has been postulated to be an important inducer of host stromal response and angiogenesis. More recently, FGFR1 amplifications were investigated using large-scale single nucleotide polymorphism arrays in lung cancer. We hypothesized that FGFR1 overexpression may be correlated with the clinicopathological features of lung cancers. The increased copy number of the FGFR1 gene was analyzed by real-time polymerase chain reaction amplifications in 100 surgically treated non-small cell lung cancer cases from Nagoya City University Hospital. Sixty-five squamous cell carcinoma cases were included. An increased FGFR1 gene copy number was found in 32 (32%) lung cancer patients. The increased FGFR1 copy number status significantly correlated with gender (females 13.8% vs. males 39.4%, p=0.0173), smoking status (never smoker 4.2% vs. smoker 40.8%, p=0.0004) and pathological subtypes (squamous cell carcinoma 41.5% vs. non-squamous cell carcinoma 14.3%, p=0.0066). However, within the squamous cell carcinomas the FGFR1 copy number status did not significantly correlate with gender, smoking status, pathological stages and differentiation status of the lung cancers. Thus, the FGFR1 copy number is common within squamous cell carcinoma.

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“…27 One therapeutic intervention in signal transduction would be the stable formation of an incomplete (nonsignaling) complex to block cell replication for the treatment of cancer. 28,29 Insulin Signaling. Obesity and diabetes is a growing health problem in the developing world.…”

Section: Fgf Signal Transductionmentioning

confidence: 99%

Role of Glycosaminoglycans in Cellular Communication

2004

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Glycosaminoglycans are of critical importance in intercellular communication in organisms. This ubiquitous class of linear polyanions interacts with a wide variety of proteins, including growth factors and chemokines, which regulate important physiological processes. The presence of glycosaminoglycans on cell membranes and in the extracellular matrix also has resulted in their exploitation by infectious pathogens to gain access and entry into animal cells. This Account examines the structural and physical characteristics of these molecules responsible for their interaction with proteins important in cell-cell communication.

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Fibroblast growth factors in cancer: therapeutic possibilities

Cited by 55 publications

References 102 publications

Long Pentraxin-3 Inhibits Epithelial–Mesenchymal Transition in Melanoma Cells

Long Pentraxin-3 Inhibits Epithelial–Mesenchymal Transition in Melanoma Cells

Increased FGFR1 copy number in lung squamous cell carcinomas

Role of Glycosaminoglycans in Cellular Communication

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