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<p>Cancer-associated fibroblasts (CAFs) play a pivotal role in breast cancer (BC) progression by modulating the tumor microenvironment through exosome-mediated interactions. CAF-derived exosomes are rich in bioactive molecules such as metabolites, proteins, and non-coding RNAs that influence metabolic reprogramming in BC cells. These exosomes facilitate the transfer of metabolic enzymes and signaling molecules that enhance glycolysis, lipid metabolism, and oxidative phosphorylation, thereby supporting tumor growth, therapy resistance, and metastasis. This review highlights the molecular mechanisms underlying the role of CAF-derived exosomes in BC metabolism, with a focus on their contributions to metabolic plasticity and tumor progression. Potential therapeutic strategies targeting CAF exosome biogenesis, release, or uptake will also be discussed to shed light on innovative approaches for disrupting this metabolic symbiosis.</p> Graphical abstract <p></p>

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CAF-derived exosomes: orchestrators of dysregulated signaling pathways in breast cancer progression

  • 期刊论文

  • 发表日期：

    2025年9月27日

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  • Almuthana K. Hameed,
  • Safia Obaidur Rab,
  • Thanaa Amir Ahmed,
  • Muktesh Chandra,
  • Jaafaru Sani Mohammed,
  • Renukajyothi S.,
  • Priya Priyadarshini Nayak,
  • Prakhar Tomar,
  • Ahmed Hussn,
  • Abbas Fadhel Ali

摘要

Cancer-associated fibroblasts (CAFs) play a pivotal role in breast cancer (BC) progression by modulating the tumor microenvironment through exosome-mediated interactions. CAF-derived exosomes are rich in bioactive molecules such as metabolites, proteins, and non-coding RNAs that influence metabolic reprogramming in BC cells. These exosomes facilitate the transfer of metabolic enzymes and signaling molecules that enhance glycolysis, lipid metabolism, and oxidative phosphorylation, thereby supporting tumor growth, therapy resistance, and metastasis. This review highlights the molecular mechanisms underlying the role of CAF-derived exosomes in BC metabolism, with a focus on their contributions to metabolic plasticity and tumor progression. Potential therapeutic strategies targeting CAF exosome biogenesis, release, or uptake will also be discussed to shed light on innovative approaches for disrupting this metabolic symbiosis.

Graphical abstract