Related Experiment Video
Updated: Feb 22, 2026

Engineering Artificial Factors to Specifically Manipulate Alternative Splicing in Human Cells
Published on: April 26, 2017
Role of fibroblast growth factor receptor-2 splicing in normal and cancer cells
1Division of Aging and Carcinogenesis, Research Team for Geriatric Pathology, Tokyo Metropolitan Institute of Gerontology, Tokyo 173-0015, Japan, tishiwat@tmig.or.jp.
Abstract:
Types 1-4 of fibroblast growth factor receptors (FGFR) are all expressed in various cancers. Because of its prominent role in carcinogenesis and cancer progression, FGFR-2, is being considered as a novel target in cancer treatment. Owing to the alternative splicing of its extracellular domain, FGFR-2 exists in two variants: IIIb and IIIc. FGFR-2 IIIb is mainly expressed in normal epithelial cells, as well as in oral mucosal, esophageal, gastric, colorectal, pancreatic, pulmonary, breast, endometrial, cervical, and prostate cancers. The IIIc variant of FGFR is expressed in mesenchymal cells, and during epithelial-mesenchymal transition (EMT), is expressed in colorectal, pancreatic, bladder, cervical, and prostate cancers. The FGFR IIIb and IIIc variants bind different forms of FGFs and exert autocrine and/or paracrine effects in cancers. Recent reports indicate that switching from IIIb to IIIc variants correlates with the aggressiveness of the cancers via EMT. Here, we discuss the expression, role, and regulatory mechanisms of IIIb and IIIc variants of FGFR in cancers.
Insights
Fibroblast growth factor receptor-2 (FGFR-2) variants, IIIb and IIIc, are key in cancer progression. Their expression and switching correlate with cancer aggressiveness, making FGFR-2 a potential therapeutic target.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- Fibroblast growth factor receptors (FGFRs) are implicated in various cancers.
- FGFR-2 is a significant factor in carcinogenesis and cancer progression.
- FGFR-2 is a potential novel therapeutic target in cancer treatment.
Purpose of the Study:
- To discuss the expression patterns of FGFR-2 variants IIIb and IIIc in different cancers.
- To elucidate the roles of FGFR-2 variants in cancer development and progression.
- To explore the regulatory mechanisms governing FGFR-2 variant expression and function in cancer.
Main Methods:
- Review of scientific literature on FGFR-2 expression and function in cancer.
- Analysis of alternative splicing mechanisms leading to FGFR-2 IIIb and IIIc variants.
- Examination of the correlation between FGFR-2 variant switching and epithelial-mesenchymal transition (EMT).
Main Results:
- FGFR-2 IIIb is expressed in normal epithelial cells and numerous epithelial cancers.
- FGFR-2 IIIc is expressed in mesenchymal cells and certain cancers, particularly during EMT.
- Switching from FGFR-2 IIIb to IIIc correlates with increased cancer aggressiveness via EMT.
Conclusions:
- FGFR-2 variants IIIb and IIIc exhibit distinct expression profiles in normal tissues and cancers.
- The differential expression and switching of FGFR-2 variants play critical roles in cancer progression.
- Understanding FGFR-2 variant regulation offers insights into targeted cancer therapies.
More Related Videos
Related Concept Videos
RNA Splicing
Mitogens and the Cell Cycle
Abnormal Proliferation
mTOR Signaling and Cancer Progression
The mTOR pathway or the...
Alternative RNA Splicing
There are five types of alternative RNA splicing that vary in the ways the pre-mRNA segments are removed or retained in the mature mRNA. The first...
TGF - β Signaling Pathway

