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<p>The intricate interplay within the tumor microenvironment (TME) significantly dictates the trajectory of cancer progression and therapeutic response. In HER2-positive breast cancer, a particularly aggressive subtype, cancer-associated fibroblasts (CAFs) emerge as pivotal stromal components, actively orchestrating malignant behaviors. Concurrently, microRNAs (miRNAs), small non-coding RNAs, serve as potent post-transcriptional regulators and critical mediators of intercellular communication, often encapsulated within exosomes. This review provides a comprehensive analysis of the reciprocal miRNA-mediated modulation between HER2-positive breast cancer cells and CAFs. It elucidates how tumor cell-derived miRNAs reprogram normal fibroblasts into pro-tumorigenic CAFs, and how CAF-derived miRNAs, in turn, influence HER2-positive cancer cell proliferation, invasion, metastasis, and crucially, resistance to HER2-targeted therapies. Understanding this dynamic axis reveals a self-sustaining feedback loop that drives disease advancement and therapeutic evasion. This synthesis underscores the immense potential of targeting these complex miRNA-CAF interactions as a novel strategy for diagnostic, prognostic, and therapeutic interventions, aiming to overcome the persistent challenge of resistance in HER2-positive breast cancer.</p>

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MicroRNA-mediated modulation of cancer-associated fibroblasts in HER2-positive breast tumor microenvironment: a comprehensive review

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年1月28日

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  • Mustafa T. Ardah,
  • Waleed K. Abdulsahib,
  • Hasanain Amer Naji,
  • S. Renuka Jyothi,
  • Samir Sahoo,
  • J. Bethanney Janney,
  • Vipasha Sharma,
  • Aashna Sinha,
  • Mohigul Kholiyeva

摘要

The intricate interplay within the tumor microenvironment (TME) significantly dictates the trajectory of cancer progression and therapeutic response. In HER2-positive breast cancer, a particularly aggressive subtype, cancer-associated fibroblasts (CAFs) emerge as pivotal stromal components, actively orchestrating malignant behaviors. Concurrently, microRNAs (miRNAs), small non-coding RNAs, serve as potent post-transcriptional regulators and critical mediators of intercellular communication, often encapsulated within exosomes. This review provides a comprehensive analysis of the reciprocal miRNA-mediated modulation between HER2-positive breast cancer cells and CAFs. It elucidates how tumor cell-derived miRNAs reprogram normal fibroblasts into pro-tumorigenic CAFs, and how CAF-derived miRNAs, in turn, influence HER2-positive cancer cell proliferation, invasion, metastasis, and crucially, resistance to HER2-targeted therapies. Understanding this dynamic axis reveals a self-sustaining feedback loop that drives disease advancement and therapeutic evasion. This synthesis underscores the immense potential of targeting these complex miRNA-CAF interactions as a novel strategy for diagnostic, prognostic, and therapeutic interventions, aiming to overcome the persistent challenge of resistance in HER2-positive breast cancer.