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Updated: Feb 18, 2026
Screening for Melanoma Modifiers using a Zebrafish Autochthonous Tumor Model
Published on: November 13, 2012
FGF5 is expressed in melanoma and enhances malignancy in vitro and in vivo
Sara Ghassemi1, Katharina Vejdovszky1, Emine Sahin1
1Institute of Cancer Research, Department of Medicine I, Comprehensive Cancer Center Vienna, Medical University of Vienna, Vienna, Austria.
Abstract:
Although FGF5 mRNA was previously found expressed in some melanoma cell lines in contrast to normal human melanocytes, neither its contribution to melanoma growth nor its expression in melanoma tissue has been investigated. Here we demonstrate that ectopic overexpression of FGF5 in human melanoma cells with low endogenous FGF5 expression increased clonogenicity and invasion but not short-term growth in vitro. Silencing of FGF5 in melanoma cells with high endogenous FGF5 expression had the opposite effect on clonogenicity. FGF overexpression led to increased signaling along the MAPK and NFAT axis but had no effect on STAT3 signaling. In an in vivo experiment in immunocompromised mice, human melanoma xenografts overexpressing FGF5 showed enhanced tumor growth, a higher Ki-67 proliferation index, decreased apoptosis and enhanced angiogenesis. Immunohistochemistry performed on a tissue microarray demonstrated FGF5 protein expression in more than 50% of samples of melanoma and benign nevi. These data suggest that FGF5 has oncogenic potential in melanoma cells and contributes to melanoma growth in a subset of patients. This highlights the importance of further evaluating FGF5 as potential biomarker and therapy target in melanoma.
Insights
Fibroblast Growth Factor 5 (FGF5) promotes melanoma cell invasion and tumor growth. FGF5 may serve as a potential biomarker and therapeutic target for melanoma patients.
Area of Science:
- Oncology
- Molecular Biology
- Dermatology
Background:
- Fibroblast Growth Factor 5 (FGF5) mRNA is detected in melanoma cell lines, but its role in melanoma development and tissue expression remains unclear.
- Previous studies noted FGF5 mRNA expression in melanoma cell lines, contrasting with normal melanocytes, prompting further investigation into its functional significance.
Purpose of the Study:
- To investigate the functional role of FGF5 in melanoma cell behavior, including clonogenicity, invasion, and growth.
- To examine the effect of FGF5 on intracellular signaling pathways (MAPK, NFAT, STAT3).
- To assess FGF5 expression in melanoma tissues and its correlation with tumor characteristics.
Main Methods:
- Ectopic overexpression and silencing of FGF5 in human melanoma cell lines.
- In vitro assays for clonogenicity, invasion, and short-term growth.
- Western blot analysis for MAPK, NFAT, and STAT3 signaling.
- In vivo studies using human melanoma xenografts in immunocompromised mice.
- Immunohistochemistry on a melanoma tissue microarray.
Main Results:
- FGF5 overexpression enhanced melanoma cell clonogenicity and invasion in vitro.
- FGF5 silencing reduced clonogenicity in high-FGF5 expressing melanoma cells.
- FGF5 overexpression activated MAPK and NFAT signaling pathways.
- In vivo, FGF5 overexpression led to increased tumor growth, proliferation, angiogenesis, and decreased apoptosis.
- FGF5 protein was expressed in over 50% of melanoma and benign nevus samples.
Conclusions:
- FGF5 exhibits oncogenic potential in melanoma, contributing to tumor growth, invasion, and angiogenesis.
- FGF5 signaling influences key pathways involved in melanoma progression.
- FGF5 is expressed in a significant proportion of melanoma and benign nevi, suggesting its potential as a biomarker.
- FGF5 warrants further evaluation as a therapeutic target for melanoma.
