Aberrant Expression of FGFRL1 in Esophageal Cancer and Its Regulation by miR-107
Related Experiment Video
Updated: Aug 1, 2025

Induction of Mesenchymal-Epithelial Transitions in Sarcoma Cells
Published on: April 7, 2017
Priyanka Sharma1,2, Vaishali Kaushik1, Anoop Saraya3
1University School of Biotechnology, Guru Gobind Singh Indraprastha University, Dwarka, New Delhi, India.
Background:
Fibroblast growth factor receptors are growth factor receptor tyrosine kinases, exerting their roles in embryogenesis, tissue homeostasis, and development of cancer. However, little is known about the expression and function of FGFRL1 in esophageal cancer (EC).
Methods:
We systematically evaluated the expression of FGFRL1 in TCGA and GETex datasets followed by expression analysis in EC cell lines and clinical specimens using immunofluorescence (IF) and immunohistochemistry (IHC) respectively.
Results:
GEPIA analysis on TCGA and GETex datasets identified significant upregulation of FGFRL1 in EC patients (n=182) compared to normal controls (n=286, p<0.05). IHC analysis showed significantly higher FGFRL1 expression in EC tissues as compared to the distant matched non-malignant tissues (p<0.001). Immunoflourescence in EC cells suggested increased expression of FGFRL1 from WDSCC (KYSE30) to MDSCC (KYSE140) and finally to PDSCC (KYSE410). In-silico tools predicted miR-107 as most significant miRNA regulating FGFRL1 expression. qRT-PCR revealed miR-107 expression to be significantly and inversely correlated with FGFRL1 expression in 73% (22/30) EC tissues (p=0.015) and over-expression of miR-107 resulted in significantly decreased expression of FGFRL1 at mRNA (fold change=0.11, p=0.0016) as well as protein level in miR-107 versus NC treated cells. Luciferase reporter assay using FGFRL1-3'UTR further confirmed it to be a direct target of miR-107.
Conclusion:
Our results herein document clinical as well as functional relevance of FGFRL1 in EC and its regulation by miR-107.
Insights
Fibroblast growth factor receptor like 1 (FGFRL1) is upregulated in esophageal cancer (EC). MiR-107 directly targets and downregulates FGFRL1, indicating a clinical and functional role in EC development.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Fibroblast growth factor receptors (FGFRs) are tyrosine kinases crucial for development and cancer.
- The expression and function of FGFRL1 in esophageal cancer (EC) remain largely uncharacterized.
Purpose of the Study:
- To investigate the expression and clinical significance of FGFRL1 in esophageal cancer.
- To identify regulatory mechanisms of FGFRL1 in EC, focusing on microRNA interactions.
Main Methods:
- Systematic evaluation of FGFRL1 expression in TCGA and GETex datasets.
- Immunofluorescence and immunohistochemistry for FGFRL1 in EC cell lines and clinical tissues.
- In-silico prediction, qRT-PCR, and luciferase reporter assays to analyze miR-107 regulation of FGFRL1.
Main Results:
- FGFRL1 was significantly upregulated in EC tissues and cell lines compared to normal controls.
- FGFRL1 expression increased with EC progression (WDSCC to PDSCC).
- MiR-107 was identified as a direct regulator of FGFRL1, inversely correlated with its expression and significantly downregulating it at both mRNA and protein levels.
Conclusions:
- FGFRL1 plays a significant clinical and functional role in esophageal cancer.
- MiR-107 directly targets and downregulates FGFRL1, suggesting a novel regulatory axis in EC.
Related Concept Videos
Mitogens and the Cell Cycle
Abnormal Proliferation
Receptor Downregulation in MVBs
The EGFR can initiate signaling pathways that lead to cell proliferation, migration, and differentiation. Overexpression of EGFR stimulates cells to proliferate. Excessive EGFR...
Role of Ephrin-Eph Signalling in Intestinal Stem Cell Renewal
MicroRNAs
Master Transcription Regulators

