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Updated: Nov 3, 2025

A Mouse Model to Investigate the Role of Cancer-Associated Fibroblasts in Tumor Growth
06:35

A Mouse Model to Investigate the Role of Cancer-Associated Fibroblasts in Tumor Growth

Published on: December 22, 2020

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Fibroblast Growth Factor Receptors (FGFRs) and Noncanonical Partners in Cancer Signaling

Harriet R Ferguson1, Michael P Smith1, Chiara Francavilla1,2

  • 1Division of Molecular and Cellular Function, School of Biological Science, Faculty of Biology Medicine and Health (FBMH), The University of Manchester, Manchester M13 9PT, UK.

Cells
|June 2, 2021
PubMed

Insights

Fibroblast Growth Factor (FGF)/FGF receptor (FGFR) signaling is crucial in cancer, with aberrant FGFR signaling observed in many cancer types. Its diverse interactions suggest a significant role in cancer progression, independent of genetic mutations.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Signaling Pathways

Background:

  • Targeted cancer therapies are context-dependent, influenced by tumor signaling pathways and cell-type crosstalk.
  • The Fibroblast Growth Factor (FGF)/FGF receptor (FGFR) signaling axis is a key example of context-dependent signaling in cancer.
  • Aberrant FGFR signaling is prevalent across numerous cancer types, including lung, breast, glioblastoma, prostate, and gastrointestinal cancers.

Purpose of the Study:

  • To review the role of Fibroblast Growth Factor (FGF)/FGF receptor (FGFR) signaling in cancer.
  • To highlight the context-dependent nature of FGFR signaling in cancer progression.
  • To explore the diverse signaling partners and mechanisms of FGFR in cancer.

Main Methods:

  • Literature review of studies on FGF/FGFR signaling in various cancers.
  • Analysis of genetic aberrations (amplification, overexpression, mutations, translocations) in FGFR1-4.
  • Investigation of canonical and noncanonical FGFR signaling pathways and interactions.

Main Results:

  • FGFR signaling is frequently dysregulated in cancer, primarily via FGFR1 and FGFR2 amplification/overexpression leading to ligand-independent activation.
  • Mutations and translocations of FGFR1-4 are also implicated in cancer development.
  • Noncanonical interactions with cell adhesion molecules, extracellular matrix proteins, and other receptor tyrosine kinases contribute to cancer cell invasion, migration, angiogenesis, therapy resistance, and metastasis.

Conclusions:

  • FGFR signaling plays a significant role in cancer progression through both canonical and noncanonical pathways.
  • The diverse interactions of FGFR with various cellular components underscore its importance in cancer, irrespective of direct genetic alterations.
  • Understanding FGFR signaling complexity is vital for developing effective, context-aware targeted cancer therapies.
Keywords:
EGFRFGFRsFGFscancercell adhesion moleculescoreceptorsextracellular matrixreceptor tyrosine kinasesignalingtumorigenesis

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