Abstract
Gastric cancer (GC) is a leading cause of cancer-related deaths worldwide, and therapeutic options for advanced GC are limited. Here, we observe that intratumoral microbiota controls chemokine expression, which in turn recruits immune cells into the tumor, and that immune infiltration is strongly associated with patient survival and disease attributes. Furthermore, microbiota regulation of chemokines is differentiated in GC patients with different survival risks. As seen in gastric tumors, in high-survival-risk patients, Pseudomonas regulates CCL4, CXCL9, CXCL10, and CXCL11 accumulation to recruit immune cells such as CD4+ T cells, CD8+ T cells, and M1 macrophages. In low-survival-risk patients, Leptospira regulates CCL4, CCL5, CXCL9, and CXCL10 accumulation to recruit multiple types of immune cells. An independent single-cell dataset of GC verified the relationship between chemokines and immune cells. What's more, chemokines, including CCL4, CCL5, CXCL9, CXCL10, and CXCL11, strongly influence the sensitivity of GC patients to potential drug candidates. This study demonstrates that intratumoral microbiota closely influences the gastric immune microenvironment and that this molding has prognostic heterogeneity, opening avenues for cancer prevention and therapy.
Published Version
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