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<p>While numerous studies have reported that intratumor bacteria modulate tumor biological characteristics and therapeutic outcomes, the role of intracellular bacteria in gastrointestinal tumor (GIT) progression remains largely unexplored. Here, we show, through bioinformatics prediction and consecutive patient sample validation, that Stenotrophomonas is associated with tumor progression and poor prognosis in GIT. Using various murine tumor models, we find that intracellular Stenotrophomonas promotes GIT progression by decreasing IFNβ secretion and inhibiting MHC-II<sup>+</sup> macrophages, thereby impairing the activity of effector CD8<sup>+</sup> T cells. Mechanistically, Stenotrophomonas entry into tumor cells induces endoplasmic reticulum stress, degrades STING protein, and downregulates the type I IFN pathway response. Additionally, Stenotrophomonas contributes to resistance to immunotherapy in GIT, which can be reversed by levofloxacin. Our findings indicate that intracellular Stenotrophomonas within tumor cells plays an important role in promoting GIT progression and poor prognosis and could serve as a potential target to improve outcomes for patients with GIT.</p>

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Stenotrophomonas promotes gastrointestinal tumor progression via STING degradation in tumour cells and mitigated immune response

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年1月26日

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  • Huolun Feng,
  • Kunling Chen,
  • Zhihui Xi,
  • Baijin Xia,
  • Xi Chen,
  • Yiqin Huang,
  • Zuda Huang,
  • Jieqing Guo,
  • Dandan Zhu,
  • Fa Ling,
  • Jianlong Zhou,
  • Yuhan Zhang,
  • Yucheng Zhang,
  • Yongfeng Liu,
  • Wenxing Zhang,
  • Jiatong Lin,
  • Zejian Lyu,
  • Qunsheng Huang,
  • Junjiang Wang,
  • Tieying Hou,
  • Jiabin Zheng,
  • Fan Xing,
  • Yong Li

摘要

While numerous studies have reported that intratumor bacteria modulate tumor biological characteristics and therapeutic outcomes, the role of intracellular bacteria in gastrointestinal tumor (GIT) progression remains largely unexplored. Here, we show, through bioinformatics prediction and consecutive patient sample validation, that Stenotrophomonas is associated with tumor progression and poor prognosis in GIT. Using various murine tumor models, we find that intracellular Stenotrophomonas promotes GIT progression by decreasing IFNβ secretion and inhibiting MHC-II+ macrophages, thereby impairing the activity of effector CD8+ T cells. Mechanistically, Stenotrophomonas entry into tumor cells induces endoplasmic reticulum stress, degrades STING protein, and downregulates the type I IFN pathway response. Additionally, Stenotrophomonas contributes to resistance to immunotherapy in GIT, which can be reversed by levofloxacin. Our findings indicate that intracellular Stenotrophomonas within tumor cells plays an important role in promoting GIT progression and poor prognosis and could serve as a potential target to improve outcomes for patients with GIT.