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FGF2: a novel druggable target for glioblastoma?
Ana Jimenez-Pascual1, Kelly Mitchell2,3, Florian A Siebzehnrubl1
1European Cancer Stem Cell Research Institute, Cardiff University School of Biosciences, Cardiff, UK.
Abstract:
Introduction: Fibroblast growth factors (FGFs) are key mitogens in tissue homeostasis and cancer. FGF2 regulates self-renewal of multiple stem-cell types, is widely used in stem cell culture paradigms and has been adopted for cultivating the growth of cancer stem cells ex vivo. Research has shed light on the functions of FGF2 in brain tumors, particularly malignant glioma, and this has demonstrated that FGF2 increases self-renewal of glioblastoma stem cells.Areas covered: This review examines the potential targeting of FGF2 signaling as a possible treatment avenue for glioblastoma. The expression of FGF ligands and the FGFR family of receptor tyrosine kinases in the normal brain and in glioblastoma is described. Moreover, the paper sheds light on FGF/FGFR signaling, including the function of heparin/heparan sulfate proteoglycans in facilitating FGF signaling. We speculate on potential avenues for the therapeutic targeting of the FGF2-FGF receptor signaling axis in glioblastoma and the associated challenges envisioned with these approaches.Expert opinion: Precision targeting of FGF/FGFR signaling could improve prospective glioblastoma therapeutics and moderate adverse effects. Shrewd development of experimental models and FGF2 inhibitors could provide a 'pharmacological toolbox' for targeting diverse ligand/receptor combinations.
Insights
Targeting Fibroblast Growth Factor 2 (FGF2) signaling may offer a new treatment for glioblastoma. Inhibiting FGF2 and its receptors could improve therapies and reduce side effects for brain tumor patients.
Area of Science:
- Oncology
- Molecular Biology
- Neuroscience
Background:
- Fibroblast Growth Factors (FGFs) are crucial for tissue maintenance and cancer.
- FGF2 specifically promotes self-renewal in stem cells, including cancer stem cells, and is implicated in glioblastoma growth.
- Understanding FGF2's role in glioblastoma is vital for developing targeted therapies.
Purpose of the Study:
- To review the potential of targeting FGF2 signaling for glioblastoma treatment.
- To describe FGF ligand and FGF Receptor (FGFR) expression in normal brain and glioblastoma.
- To explore therapeutic strategies and challenges for targeting the FGF2-FGFR axis.
Main Methods:
- Literature review of FGF/FGFR signaling in glioblastoma.
- Analysis of FGF ligand and FGFR expression patterns.
- Discussion of therapeutic targeting strategies and their challenges.
Main Results:
- FGF2 signaling is active in glioblastoma and promotes cancer stem cell self-renewal.
- FGF ligands and FGFRs are expressed in both normal brain and glioblastoma.
- Heparin/heparan sulfate proteoglycans play a role in facilitating FGF signaling.
Conclusions:
- Targeting FGF/FGFR signaling presents a promising therapeutic avenue for glioblastoma.
- Precision targeting could enhance treatment efficacy and minimize adverse effects.
- Developing novel FGF2 inhibitors and experimental models is crucial for clinical translation.
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