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Updated: Apr 28, 2026

Screening and Identification of Small Peptides Targeting Fibroblast Growth Factor Receptor2 using a Phage Display Peptide Library
Published on: September 30, 2019
A novel decoy receptor fusion protein for FGF-2 potently inhibits tumour growth
1School of Life Sciences and Technology, Tongji University, 1239 Siping Road, Shanghai 200092, China.
Background:
Antiangiogenic therapies have been proven effective in cancer treatment. Fibroblast growth factor-2 (FGF-2) has been functionally implicated in tumour angiogenesis and is an important target of antiangiogenic therapies. The aim of this work was to develop a novel FGF-2 inhibitor for cancer therapy.
Methods:
Eleven fusion proteins were developed by fusing various truncated extracellular regions of FGFR1 with the Fc region of IgG1. The optimal decoy receptor fusion protein with the highest binding affinity for FGF-2 was identified by an FGF-2-binding assay and its potential antitumour effects were investigated.
Results:
We obtained a soluble decoy receptor fusion protein with the highest binding activity for FGF-2, named FGF-Trap. Fibroblast growth factor-Trap significantly abolished FGF-2-stimulated activation of FGF signalling as demonstrated by its suppression of FGF-2-mediated phosphorylation of Erk1/2 and Akt, upregulation of cyclins D1 and E and the increase in mRNA levels of vascular endothelial growth factor R1 and R2 (VEGFR1 and VEGFR2). Furthermore, FGF-Trap effectively suppressed FGF-2-induced proliferation and migration of human umbilical vein endothelial cells (HUVECs) in vitro. Most importantly, FGF-Trap potently inhibited tumour growth and angiogenesis in Caki-1 and A549 xenograft models in vivo.
Conclusions:
Fibroblast growth factor-Trap potently inhibits tumour growth by blocking FGF-2 signalling pathways and could be an effective therapeutic agent for cancer patients.
Insights
A novel fusion protein, Fibroblast growth factor-Trap, effectively inhibits tumor growth by blocking Fibroblast growth factor-2 (FGF-2) signaling. This targeted antiangiogenic therapy shows promise for cancer treatment.
Area of Science:
- Oncology
- Molecular Biology
- Biotechnology
Background:
- Antiangiogenic therapies are crucial for cancer treatment.
- Fibroblast growth factor-2 (FGF-2) drives tumor angiogenesis and is a key therapeutic target.
- Developing novel FGF-2 inhibitors is essential for advancing cancer therapy.
Purpose of the Study:
- To develop a novel fusion protein inhibitor targeting FGF-2.
- To identify a decoy receptor fusion protein with high binding affinity for FGF-2.
- To evaluate the anti-tumorigenic potential of the developed inhibitor.
Main Methods:
- Eleven fusion proteins were engineered by combining FGFR1 extracellular regions with the IgG1 Fc region.
- An FGF-2 binding assay identified the optimal decoy receptor fusion protein.
- In vitro and in vivo studies assessed the anti-tumorigenic effects of the lead candidate.
Main Results:
- A soluble decoy receptor fusion protein, FGF-Trap, with high FGF-2 binding activity was developed.
- FGF-Trap suppressed FGF-2-mediated signaling, including Erk1/2 and Akt phosphorylation, and VEGFR expression.
- FGF-Trap inhibited endothelial cell proliferation and migration in vitro and suppressed tumor growth and angiogenesis in vivo.
Conclusions:
- FGF-Trap effectively inhibits tumor growth by blocking FGF-2 signaling pathways.
- This novel therapeutic agent demonstrates significant potential for treating cancer patients.
- Targeting FGF-2 with engineered fusion proteins offers a promising antiangiogenic strategy.
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