<p>Ferroptosis, a form of regulated cell death characterized by the accumulation of lipid peroxides, has emerged as a crucial player in cancer biology, particularly in breast cancer. This review article explores the intricate regulation of ferroptosis by non-coding RNAs (ncRNAs) within the breast cancer tumor microenvironment (TME). We delve into the mechanisms through which various classes of ncRNAs, including microRNAs, long non-coding RNAs, and circular RNAs, modulate the ferroptotic response in breast cancer cells. Furthermore, we examine the interactions between ferroptosis and the TME, specifically focusing on cancer-associated fibroblasts (CAFs) and tumor-associated macrophages (TAMs). By highlighting the bidirectional relationships between these components, we aim to elucidate how the modulation of ferroptosis by ncRNAs can influence the behavior of CAFs and TAMs, ultimately impacting tumor progression and therapeutic response. This comprehensive overview underscores the potential of targeting ncRNA-mediated regulation of ferroptosis as a novel therapeutic strategy in breast cancer treatment, with implications for enhancing the efficacy of existing therapies and improving patient outcomes.</p>

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Ferroptosis and non-coding RNAs in breast cancer: insights into CAF and TAM interactions

  • Mohamed J. Saadh,
  • Ashok Kumar Bishoyi,
  • Suhas Ballal,
  • Abhayveer Singh,
  • Anita Devi,
  • Girish Chandra Sharma,
  • Abdusamat Valiev,
  • K. Satyam Naidu,
  • Pushpa Negi Bhakuni,
  • Fadhil Faez Sead

摘要

Ferroptosis, a form of regulated cell death characterized by the accumulation of lipid peroxides, has emerged as a crucial player in cancer biology, particularly in breast cancer. This review article explores the intricate regulation of ferroptosis by non-coding RNAs (ncRNAs) within the breast cancer tumor microenvironment (TME). We delve into the mechanisms through which various classes of ncRNAs, including microRNAs, long non-coding RNAs, and circular RNAs, modulate the ferroptotic response in breast cancer cells. Furthermore, we examine the interactions between ferroptosis and the TME, specifically focusing on cancer-associated fibroblasts (CAFs) and tumor-associated macrophages (TAMs). By highlighting the bidirectional relationships between these components, we aim to elucidate how the modulation of ferroptosis by ncRNAs can influence the behavior of CAFs and TAMs, ultimately impacting tumor progression and therapeutic response. This comprehensive overview underscores the potential of targeting ncRNA-mediated regulation of ferroptosis as a novel therapeutic strategy in breast cancer treatment, with implications for enhancing the efficacy of existing therapies and improving patient outcomes.