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Intratumoral bacteria are an under-researched but influential component of the cancer ecosystem, playing a key role in cancer progression. In PyMT breast tumors, we found that intracellular bacteria reside in the cytoplasm of cancer cells, promoting metastasis by triggering the accumulation of cytosolic double-stranded DNA (dsDNA), thereby activating the tumor-intrinsic cGAS-STING-interleukin (IL)-17B pathway and redirecting neutrophils toward a tumor phenotype that suppresses cytotoxic T cells.By contrast, when the same bacterial strain exists extracellularly, it can induce anti-tumor neutrophil activity without activating the STING pathway. From a physiological perspective, eliminating intracellular bacteria, or therapeutically introducing extracellular bacterial components, can relieve immunosuppression and prevent postoperative metastatic recurrence, especially in preclinical models. Clinically, the bacterial invasion features we developed are associated with poor prognosis in breast cancer patients. In summary, the spatial interactions between bacteria and host cells in metastatic niches can shape divergent tumor immunity, highlighting that the association between bacteria and the host is a key determinant of cancer immune regulation and a potential therapeutic target.
