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Absence of fibroblast growth factor 2 does not prevent tumor formation originating from the RPE
Alessandro Foletti1, Julien Ackermann, Andrea Schmidt
1ISREC (Swiss Institute for Experimental Cancer Research), Chemin des Boveresses 155, CH-1066 Epalinges, Switzerland.
Abstract:
We have analysed the importance of fibroblast growth factor 2 (FGF2) in tumor development. In a transgenic mouse model (Tyrp1-Tag) tumors form in the retinal pigment epithelium (RPE), invade surrounding tissues, and metastasize to lymph node and spleen. To address whether RPE tumor formation is dependent on FGF2, we generated FGF2-deficient mice. Such mice appeared healthy and exhibited no impairment of growth or development. Tyrp1-Tag transgenic mice, which are lacking FGF2 (FGF2-/-) developed RPE tumors that metastasize to spleen and lymph nodes. Tumor growth and survival rate are identical to Tyrp1-Tag transgenic littermates expressing FGF2. Cell lines were isolated from RPE tumors of wild-type and FGF2-deficient mice. They grow in culture, are pigmented and form vascularized tumors, when injected subcutaneously into nude mice of either FGF2-/- or FGF2+/+ genetic background. Kinetics of tumor growth was identical and independent of presence of FGF2. Together, these results demonstrate that FGF2 is not essential for tumor formation of the RPE thus suggesting that tumor growth in general may not be dependent on FGF2.
Insights
Fibroblast growth factor 2 (FGF2) is not essential for retinal pigment epithelium (RPE) tumor development or metastasis. FGF2-deficient mice show no impairment, indicating FGF2 is not critical for RPE tumor growth.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Fibroblast growth factor 2 (FGF2) role in tumor development is under investigation.
- Transgenic mouse models (Tyrp1-Tag) spontaneously develop retinal pigment epithelium (RPE) tumors with metastatic potential.
Purpose of the Study:
- To determine if FGF2 is essential for RPE tumor formation and metastasis.
- To investigate the impact of FGF2 deficiency on tumor growth kinetics and survival rates.
Main Methods:
- Generation of FGF2-deficient (FGF2-/-) mice.
- Crossbreeding FGF2-/- mice with Tyrp1-Tag transgenic mice to create RPE tumor models lacking FGF2.
- Isolation and characterization of RPE tumor cell lines from both wild-type and FGF2-deficient mice.
- Subcutaneous injection of tumor cells into nude mice to assess tumor formation and growth.
Main Results:
- FGF2-deficient mice are healthy, with normal growth and development.
- Tyrp1-Tag mice lacking FGF2 developed RPE tumors that metastasized to the spleen and lymph nodes.
- Tumor growth and survival rates in FGF2-deficient Tyrp1-Tag mice were identical to those expressing FGF2.
- RPE tumor cell lines derived from FGF2-deficient mice formed vascularized tumors in vivo, independent of FGF2 presence.
Conclusions:
- FGF2 is not essential for the initiation or progression of RPE tumors.
- Tumor growth and metastasis in this model are independent of FGF2.
- These findings suggest that FGF2 may not be a critical factor for tumor growth in general.