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REVIEW article

Front. Oncol.
Sec. Cancer Molecular Targets and Therapeutics
Volume 14 - 2024 | doi: 10.3389/fonc.2024.1415820

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

Provisionally accepted
Jinhao Chen Jinhao Chen Chunyu Cao Chunyu Cao *Hongyan Wu Hongyan Wu *Qianru Wang Qianru Wang
  • China Three Gorges University, Yichang, China

The final, formatted version of the article will be published soon.

    Triple-negative breast cancer(TNBC)is one of the subtypes with the worst prognosis due to tumour heterogeneity and lack of appropriate treatment. This condition is a consequence of the distinctive tumour microenvironment (TME). The TME is associated with factors such as the promotion of proliferation, angiogenesis, inhibition of apoptosis, suppression of the immune system and drug resistance. Therefore, remodelling the TME is critical for the treatment of TNBC. A key role in the formation of the TME is played by the fibroblast growth factor/fibroblast growth factor receptor(FGF/FGFR) signalling pathway. Thus, the FGFRs may be a potential target for treating TNBC. Over-activated FGFRs promote growth, migration and drug resistance in TNBC by influencing the onset of TME events, tumour angiogenesis and immune rejection. A thorough comprehension of the FGF/FGFR signalling pathway's mechanism of action in the development of TNBC could offer valuable insights for discovering new therapeutic strategies and drug targets.Inhibiting the FGF/FGFR axis could potentially hinder the growth of TNBC and its drug resistance by disrupting crucial biological processes in the TME, such as angiogenesis and immune evasion. This review evaluates the potential of inhibiting the FGF/FGFR axis as a strategy for treating TNBC.It explores the prospects for developing related therapeutic approaches. This study explores the research and application prospects of the FGF/FGFR axis in TNBC. The aim is to provide guidance for further therapeutic research and facilitate the development of innovative approaches targeting TNBC.

    Keywords: TNBC, FGF/FGFR pathway, Tumor Microenvironment, targeted therapies, FGFR inhibitor

    Received: 11 Apr 2024; Accepted: 02 Sep 2024.

    Copyright: © 2024 Chen, Cao, Wu and Wang. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

    * Correspondence:
    Chunyu Cao, China Three Gorges University, Yichang, China
    Hongyan Wu, China Three Gorges University, Yichang, China

    Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.