Chen Jinhao, Wang Qianru, Wu Hongyan, Huang Xiaofei, Cao Chunyu
Hubei Key Laboratory of Tumor Microenvironment and Immunotherapy, China Three Gorges University, Yichang, Hubei, China.
Affiliated Renhe Hospital of China Three Gorges University, Yichang, Hubei, China.
Front Oncol. 2025 Mar 11;14:1415820. doi: 10.3389/fonc.2024.1415820. eCollection 2024.
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.
三阴性乳腺癌(TNBC)是预后最差的亚型之一,原因在于肿瘤异质性以及缺乏合适的治疗方法。这种情况是独特的肿瘤微环境(TME)导致的结果。TME与促进增殖、血管生成、抑制细胞凋亡、抑制免疫系统以及耐药性等因素相关。因此,重塑TME对于TNBC的治疗至关重要。成纤维细胞生长因子/成纤维细胞生长因子受体(FGF/FGFR)信号通路在TME的形成中起关键作用。因此,FGFRs可能是治疗TNBC的潜在靶点。过度激活的FGFRs通过影响TME事件的发生、肿瘤血管生成和免疫排斥来促进TNBC的生长、迁移和耐药性。深入了解FGF/FGFR信号通路在TNBC发展中的作用机制,可为发现新的治疗策略和药物靶点提供有价值的见解。抑制FGF/FGFR轴可能通过破坏TME中的关键生物学过程,如血管生成和免疫逃逸,来潜在地阻碍TNBC的生长及其耐药性。本综述评估了抑制FGF/FGFR轴作为治疗TNBC策略的潜力。它探讨了开发相关治疗方法的前景。本研究探索了FGF/FGFR轴在TNBC中的研究和应用前景。目的是为进一步的治疗研究提供指导,并促进针对TNBC的创新方法的开发。