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<p>Tumor-associated macrophages (TAMs) have been implicated in fostering various hallmarks of cancer progression in gastric cancer (GC). However, the intricate molecular mechanisms underlying TAM-induced chemoresistance remain incompletely understood. Exosomes emerge as key players, mediating TAM-induced resistance to cisplatin (DDP) by regulating ferroptosis. Our investigation reveals that <i>exo-miR-1911-5p</i>, delivered to GC cells from TAMs, significantly contributes to cisplatin resistance. Specifically, direct modulation of MYB by <i>MiR-1911-5p</i> leads to decreased expression of AKR1B10, a crucial factor in preventing ferroptosis. Further exploration confirms the regulation of ACC by AKR1B10. Through targeting the MYB/AKR1B10/ACC axis, exo-miR-1911-5p inhibits ferroptosis to enhances cisplatin resistance. Additionally, <i>exo-miR-1911-5p</i> promotes M2 polarization of TAMs by targeting ARHGEF3. Collectively, our findings highlight the critical role of <i>exo-miR-1911-5p</i> in mediating cisplatin resistance through modulating the cross-talk between TAMs and GC. Targeting <i>exo-miR-1911-5p</i> could represent a promising strategy for overcoming DDP resistance in GC.</p><p></p>

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Exo-miR-1911-5p regulates ferroptosis to promote macrophages M2 polarization-mediated gastric cancer cisplatin resistance via MYB/AKR1B10/ACC

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年7月15日

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  • Zihao Kong,
  • Min Zhang,
  • Hui Yuan,
  • Jiahao Liu,
  • Huaiming Sang,
  • Ping Zhao,
  • Miao Xu,
  • Chuanlong Zhu,
  • Guoxin Zhang

摘要

Tumor-associated macrophages (TAMs) have been implicated in fostering various hallmarks of cancer progression in gastric cancer (GC). However, the intricate molecular mechanisms underlying TAM-induced chemoresistance remain incompletely understood. Exosomes emerge as key players, mediating TAM-induced resistance to cisplatin (DDP) by regulating ferroptosis. Our investigation reveals that exo-miR-1911-5p, delivered to GC cells from TAMs, significantly contributes to cisplatin resistance. Specifically, direct modulation of MYB by MiR-1911-5p leads to decreased expression of AKR1B10, a crucial factor in preventing ferroptosis. Further exploration confirms the regulation of ACC by AKR1B10. Through targeting the MYB/AKR1B10/ACC axis, exo-miR-1911-5p inhibits ferroptosis to enhances cisplatin resistance. Additionally, exo-miR-1911-5p promotes M2 polarization of TAMs by targeting ARHGEF3. Collectively, our findings highlight the critical role of exo-miR-1911-5p in mediating cisplatin resistance through modulating the cross-talk between TAMs and GC. Targeting exo-miR-1911-5p could represent a promising strategy for overcoming DDP resistance in GC.