Therapies targeting triple-negative breast cancer: a perspective on anti-FGFR

Jinhao Chen1,2,3, Qianru Wang1,3, Hongyan Wu1,3

  • 1Hubei Key Laboratory of Tumor Microenvironment and Immunotherapy, China Three Gorges University, Yichang, Hubei, China.

Frontiers in Oncology
|March 26, 2025
PubMed

Insights

Targeting the fibroblast growth factor/fibroblast growth factor receptor (FGF/FGFR) pathway offers a promising strategy to combat triple-negative breast cancer (TNBC). Inhibiting this axis disrupts the tumor microenvironment, potentially overcoming treatment resistance.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Triple-negative breast cancer (TNBC) presents a poor prognosis due to tumor heterogeneity and limited treatment options.
  • The tumor microenvironment (TME) significantly influences TNBC progression, promoting proliferation, angiogenesis, immune suppression, and drug resistance.
  • The fibroblast growth factor/fibroblast growth factor receptor (FGF/FGFR) signaling pathway plays a crucial role in TME formation and TNBC development.

Purpose of the Study:

  • To evaluate the potential of inhibiting the FGF/FGFR axis as a therapeutic strategy for TNBC.
  • To explore the role of FGF/FGFR signaling in TNBC progression, including TME modulation, angiogenesis, and immune evasion.
  • To identify new therapeutic targets and strategies for TNBC treatment by understanding the FGF/FGFR pathway's mechanisms.

Main Methods:

  • This review synthesizes current research on the FGF/FGFR signaling pathway in TNBC.
  • Analysis of the impact of FGF/FGFR overactivation on TME components and TNBC characteristics.
  • Evaluation of preclinical and clinical data regarding FGF/FGFR inhibitors in TNBC models.

Main Results:

  • Overactivated FGFRs contribute to TNBC growth, migration, and drug resistance by influencing TME events.
  • Inhibition of the FGF/FGFR axis demonstrates potential in disrupting tumor angiogenesis and overcoming immune evasion.
  • Targeting FGF/FGFR signaling may hinder TNBC proliferation and enhance sensitivity to existing therapies.

Conclusions:

  • Inhibiting the FGF/FGFR axis is a viable therapeutic strategy for TNBC, addressing critical aspects of the TME.
  • Further research into FGF/FGFR pathway inhibitors could lead to innovative treatments for TNBC.
  • Understanding the FGF/FGFR mechanism provides a foundation for developing novel drugs and therapeutic approaches for TNBC.

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