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Updated: Feb 4, 2026

Development of Compendium for Esophageal Squamous Cell Carcinoma
Published on: April 12, 2024
Blocking FGFR4 exerts distinct anti-tumorigenic effects in esophageal squamous cell carcinoma
Zhongwei Xin1, Xuemin Song1, Bin Jiang1
1Department of Thoracic Surgery, Shandong Provincial Hospital affiliated to Shandong University, Jinan, Shandong, China.
Background:
The FGFR family can be activated by FGFs and plays important roles in regulating cell growth, differentiation, migration, and angiogenesis. Recent studies have suggested that FGFR4 could regulate several processes, including tumor progression. Esophageal squamous cell carcinoma (ESCC) is a malignancy with high global occurrence. However, the molecule mechanism and the potential roles of FGFR4 in ESCC remain unknown.
Methods:
Immunohistochemistry and Western blotting were used to detect FGFR4 expression in ESCC samples and cell lines. Cell counting kit-8, and clonogenic, transwell, flow cytometric, and tumor xenograft in nude mice assays were utilized to determine the effect of blocking FGFR4 in proliferation, invasion, migration, and apoptosis of ESCC cells.
Results:
FGFR4 is frequently overexpressed in ESCC tissue and cell lines. in vitro assays have shown that blocking FGFR4 by a specific blocker, H3B-6527, significantly decreases proliferation, invasion, and migration, and alters epithelial-mesenchymal transition markers in ESCC cells. In addition, FGFR4 blockade is associated with the induction of apoptosis and affects PI3K/Akt and MAPK/ERK pathways. Moreover, FGFR4 blockade could significantly inhibit the growth of xenograft tumors in vivo.
Conclusion:
Our findings suggest that blocking FGFR4 significantly suppresses the malignant behaviors of ESCC and indicate that FGFR4 is a potential target for the treatment of ESCC.
Insights
Blocking Fibroblast Growth Factor Receptor 4 (FGFR4) significantly suppresses esophageal squamous cell carcinoma (ESCC) progression by inhibiting proliferation, invasion, and migration. This research highlights FGFR4 as a promising therapeutic target for ESCC treatment.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- Fibroblast Growth Factor Receptor (FGFR) signaling is crucial for cell growth and angiogenesis.
- FGFR4's role in tumor progression is increasingly recognized, but its mechanism in Esophageal Squamous Cell Carcinoma (ESCC) is unclear.
Purpose of the Study:
- To investigate the role and potential of FGFR4 as a therapeutic target in Esophageal Squamous Cell Carcinoma (ESCC).
Main Methods:
- Detected FGFR4 expression in ESCC tissues and cell lines using immunohistochemistry and Western blotting.
- Assessed the impact of FGFR4 blockade on ESCC cell proliferation, invasion, migration, and apoptosis through various in vitro and in vivo assays, including xenografts.
Main Results:
- FGFR4 was frequently overexpressed in ESCC.
- Blocking FGFR4 with H3B-6527 reduced ESCC cell proliferation, invasion, and migration, induced apoptosis, and affected key signaling pathways (PI3K/Akt, MAPK/ERK).
- FGFR4 blockade significantly inhibited tumor growth in vivo.
Conclusions:
- FGFR4 overexpression drives malignant behaviors in ESCC.
- Targeting FGFR4 represents a potential therapeutic strategy for treating ESCC.
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