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Background <p>Ovarian cancer typically presents at an advanced stage, has a poor prognosis, and is a leading cause of cancer-related deaths in women. Extracellular vesicles (EVs) are cell membrane-derived nanoparticles that function in specific cell-to-cell communication and are under development as novel drug delivery vehicles and modulators of the tumor microenvironment. Artificial cell-derived vesicles (ACDVs) from M1 macrophages are able to repolarize macrophages from a M2 to a M1 phenotype and target tumor cells in in vitro studies. </p> Results <p>In this study, we generated engineered EVs (EEVs) by membrane disruption of M1 macrophages (MEVs) with and without cisplatin to generate cisplatin-loaded MEVs (<i>C</i>-MEVs) and empty MEVs (<i>E</i>-MEVs), which we tested in an ovarian cancer mouse xenograft model. <i>E</i>-MEVs and <i>C</i>-MEVs exhibited significantly less weight loss and equivalent activity to cisplatin, with improved activity over controls. </p> Conclusions <p>Further development of MEVs for the treatment of ovarian cancer is warranted.</p>

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M1 macrophage-engineered vesicles have anti-cancer activity in ovarian cancer

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年7月22日

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  • Connie D. Cao,
  • J. Robert McCorkle,
  • Derek B. Allison,
  • Donglin Yan,
  • Kristen S. Hill,
  • Lan Li,
  • Rani Jayswal,
  • David Schweer,
  • Charles S. Dietrich III,
  • Frederick R. Ueland,
  • Christopher I. Richards,
  • Jill M. Kolesar

摘要

Background

Ovarian cancer typically presents at an advanced stage, has a poor prognosis, and is a leading cause of cancer-related deaths in women. Extracellular vesicles (EVs) are cell membrane-derived nanoparticles that function in specific cell-to-cell communication and are under development as novel drug delivery vehicles and modulators of the tumor microenvironment. Artificial cell-derived vesicles (ACDVs) from M1 macrophages are able to repolarize macrophages from a M2 to a M1 phenotype and target tumor cells in in vitro studies.

Results

In this study, we generated engineered EVs (EEVs) by membrane disruption of M1 macrophages (MEVs) with and without cisplatin to generate cisplatin-loaded MEVs (C-MEVs) and empty MEVs (E-MEVs), which we tested in an ovarian cancer mouse xenograft model. E-MEVs and C-MEVs exhibited significantly less weight loss and equivalent activity to cisplatin, with improved activity over controls.

Conclusions

Further development of MEVs for the treatment of ovarian cancer is warranted.