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Expression and Purification of FGFR1-Fc Fusion Protein and Its Effects on Human Lung Squamous Carcinoma
Lulu Zheng1,2, Huan Liu1, Lingfeng Chen3
1School of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, Zhejiang, 325035, China.
Abstract:
Molecular-targeted therapies for lung squamous cell carcinoma (LSCC) are limited mainly because targetable oncogenic aberrations are absent in LSCC. Recent genomic analyses have revealed that the fibroblast growth factor (FGF) signaling pathway plays a fundamental role in LSCC progression via cancer cell proliferation and angiogenesis. In the present study, we designed, expressed, and purified a fibroblast growth factor receptor fragment (FGFR1-Fc) fusion protein using NS/0 cells. In FGF2-FGFR1 overexpressed NCI-H1703 cells, the FGFR1-Fc fusion protein effectively inhibited proliferation and invasion and arrested the cell cycle at the G0-G1 phase. In NCI-H1703 cells treated with the FGFR1-Fc fusion protein, the phosphorylation levels of FGFR1, FRS2, ERK, and AKT were significantly reduced. Using an siRNA assay, we demonstrated that FGF2-FGFR1 is the major anti-tumor target of FGFR1-Fc fusion the FGFR1-Fc fusion protein, which also significantly inhibited proliferation and invasion by NCI-H1703 cells via the FGF2-FGFR1 signaling pathway. In addition, the FGFR1-Fc fusion protein significantly inhibited angiogenesis in an embryonic chorioallantoic membrane model. The FGFR1-Fc fusion protein may be an effective therapeutic candidate for LSCC.
Insights
A novel fibroblast growth factor receptor fragment (FGFR1-Fc) fusion protein effectively targets lung squamous cell carcinoma (LSCC) by inhibiting cancer cell proliferation, invasion, and angiogenesis, offering a potential new therapy.
Area of Science:
- Oncology
- Molecular Biology
- Biotechnology
Background:
- Targeted therapies for lung squamous cell carcinoma (LSCC) are limited due to a lack of identifiable oncogenic drivers.
- Genomic studies highlight the fibroblast growth factor (FGF) signaling pathway's critical role in LSCC progression, influencing cancer cell proliferation and angiogenesis.
Purpose of the Study:
- To design, express, and purify a fibroblast growth factor receptor fragment (FGFR1-Fc) fusion protein.
- To evaluate the therapeutic potential of FGFR1-Fc in inhibiting LSCC progression.
Main Methods:
- A FGFR1-Fc fusion protein was produced using NS/0 cells.
- The efficacy of FGFR1-Fc was assessed in FGF2-FGFR1 overexpressed NCI-H1703 lung cancer cells, evaluating proliferation, invasion, cell cycle, and signaling pathway modulation (FGFR1, FRS2, ERK, AKT phosphorylation).
- An siRNA assay identified FGF2-FGFR1 as the primary target, and angiogenesis was evaluated using an embryonic chorioallantoic membrane model.
Main Results:
- FGFR1-Fc significantly inhibited proliferation and invasion and induced G0-G1 cell cycle arrest in NCI-H1703 cells.
- Treatment with FGFR1-Fc led to a marked reduction in the phosphorylation of FGFR1, FRS2, ERK, and AKT.
- The fusion protein demonstrated significant inhibition of angiogenesis in vivo and confirmed FGF2-FGFR1 as the key anti-tumor target.
Conclusions:
- The FGFR1-Fc fusion protein effectively targets the FGF2-FGFR1 signaling pathway in LSCC.
- FGFR1-Fc exhibits potent anti-proliferative, anti-invasive, and anti-angiogenic effects.
- This FGFR1-Fc fusion protein represents a promising therapeutic candidate for treating lung squamous cell carcinoma.
