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Updated: Apr 26, 2026

A Mouse Model to Investigate the Role of Cancer-Associated Fibroblasts in Tumor Growth
Published on: December 22, 2020
Fibroblast growth factor receptors: multifactorial-contributors to tumor initiation and progression
Shachuan Feng1, Li Zhou1, Edouard Collins Nice2
1School of life science, and The State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, P.R. China.
Abstract:
Fibroblast growth factor receptors (FGFRs), encoded by four genes (FGFR1, FGFR2, FGFR3, and FGFR4) are tightly associated with many biological processes such as organ development, cell proliferation and migration. Studies over the past decades have validated the pivotal roles FGFRs play in tumorigenesis due to the regulation of diverse tumorigenesis-related processes, including cell survival, proliferation, inflammation, metastasis and angiogenesis. Interestingly, FGFR mutations in somatic cells leading to tumorigenesis and those in germ cells leading to developmental disorders are identical, suggesting that FGFR mutations result in different diseases due to their spatio-temporal expression. Thus, discoveries in developmental biology may also be applicable to cancer. FGFRs regulate the expression and/or the activity of a myriad of molecules (e.g. matrix metalloproteinases (MMPs) and Snail) that are tightly linked to tumorigenesis by four main signaling pathways (RAS-MAPK, PI3K-AKT, PLCγ-PIP2, and STAT), as well as other minor branches. Epigenetic and genetic alteration of FGFR genes, including DNA methylation, histone remodeling, microRNA regulation, single nucleotide polymorphisms (SNPs), gene missense mutations, amplification, and fusion of FGFRs with other genes, which result in gain or loss of FGFR function, have been identified in many types of cancer. In this review, we focus in particular on recent advances in the relationship between FGFR disorders and tumorigenesis.
Insights
Fibroblast growth factor receptors (FGFRs) are crucial for development and cell functions. FGFR alterations drive cancer and developmental disorders, highlighting the link between developmental biology and tumorigenesis.
Area of Science:
- Molecular Biology
- Developmental Biology
- Oncology
Background:
- Fibroblast growth factor receptors (FGFRs) are key regulators of fundamental biological processes, including organ development, cell proliferation, and migration.
- FGFRs play critical roles in tumorigenesis by influencing cell survival, proliferation, inflammation, metastasis, and angiogenesis.
Purpose of the Study:
- To review recent advances in understanding the relationship between Fibroblast growth factor receptor (FGFR) disorders and tumorigenesis.
- To explore how identical FGFR mutations can lead to distinct diseases based on spatio-temporal expression, linking developmental biology to cancer research.
Main Methods:
- Literature review focusing on recent advances in FGFR research.
- Analysis of genetic and epigenetic alterations affecting FGFR genes and their functional consequences.
- Examination of FGFR signaling pathways involved in tumorigenesis.
Main Results:
- FGFR mutations identified in somatic and germ cells can cause both cancer and developmental disorders.
- FGFRs regulate key tumorigenesis-related molecules (e.g., MMPs, Snail) via major signaling pathways (RAS-MAPK, PI3K-AKT, PLCγ-PIP2, STAT).
- Various genetic and epigenetic alterations of FGFR genes (methylation, SNPs, mutations, amplification, fusion) lead to altered FGFR function in cancer.
Conclusions:
- FGFRs are pivotal in tumorigenesis, with their alterations contributing to various cancers.
- Understanding FGFR regulation in development offers insights into cancer mechanisms.
- Further research into FGFRs is crucial for both developmental and cancer biology.
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