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<p>High-grade serous ovarian cancer (HGSOC) is characterized by extensive transcoelomic dissemination and the accumulation of ascites. However, how site-specific tumor microenvironment (TME) drives progression remains unknown. Here we show the co-occurrence and spatial co-localization of <i>SELENOP</i><sup>+</sup> macrophages and precursor exhausted CD8<sup>+</sup> T cells and demonstrate that <i>SELENOP</i><sup>+</sup> macrophages activate T cells via selenoprotein P in vitro and in vivo. We further identify a dynamic transition in the <i>SELENOP</i><sup>+</sup>/<i>SPP1</i><sup>+</sup> macrophage populations as tumor metastasis, driven by increased hypoxia malignant epithelial cells through VEGFA-EPHB2 signaling. We also reveal that anti-VEGFA intervention controls ovarian tumor growth by increasing <i>SELENOP</i><sup>+</sup> macrophages and cytotoxicity of CD8<sup>+</sup> T cells in vivo. Taken together, these findings spotlight the role of tumor-induced TME remodeling in subverting immune-mediated tumor control and thus facilitating HGSOC metastasis in females. Collectively, our results provide a foundation for the development of targeted therapeutic interventions aimed at impeding HGSOC metastatic trajectory.</p>

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Hypoxia-driven remodeling of SELENOP+ macrophages shapes T cell dynamics and promotes ovarian cancer metastasis

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年1月12日

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  • Qing Liu,
  • Chenzhao Feng,
  • Tianhao Wu,
  • Siyang Zhang,
  • Xinyi Wang,
  • Qian Zhao,
  • Xueying Song,
  • Shuangyan Liu,
  • Linru Quan,
  • Yuli Zhang,
  • Shimin Zhang,
  • Bin Yang,
  • Jixin Li,
  • Gang Chen,
  • Xuanzhang Huang,
  • Chaoyang Sun,
  • Xin Zhou

摘要

High-grade serous ovarian cancer (HGSOC) is characterized by extensive transcoelomic dissemination and the accumulation of ascites. However, how site-specific tumor microenvironment (TME) drives progression remains unknown. Here we show the co-occurrence and spatial co-localization of SELENOP+ macrophages and precursor exhausted CD8+ T cells and demonstrate that SELENOP+ macrophages activate T cells via selenoprotein P in vitro and in vivo. We further identify a dynamic transition in the SELENOP+/SPP1+ macrophage populations as tumor metastasis, driven by increased hypoxia malignant epithelial cells through VEGFA-EPHB2 signaling. We also reveal that anti-VEGFA intervention controls ovarian tumor growth by increasing SELENOP+ macrophages and cytotoxicity of CD8+ T cells in vivo. Taken together, these findings spotlight the role of tumor-induced TME remodeling in subverting immune-mediated tumor control and thus facilitating HGSOC metastasis in females. Collectively, our results provide a foundation for the development of targeted therapeutic interventions aimed at impeding HGSOC metastatic trajectory.