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While bacterial immunomodulation has been extensively studied, the role of bacterial metabolic competition, particularly for glucose, in tumor suppression remains unclear. We aimed to investigate how engineered\n                    <jats:italic toggle=\"yes\">Salmonella<\/jats:italic>\n                    strains exploit metabolic competition to trigger antitumor immunity and improve therapeutic outcomes in bladder cancer models.\n                    <jats:bold>Methods:<\/jats:bold>\n                    Using genetic screening, we generated a gluconeogenesis-deficient\n                    <jats:italic toggle=\"yes\">Salmonella<\/jats:italic>\n                    strain, the AISIH strain with the\n                    <jats:italic toggle=\"yes\">glpX<\/jats:italic>\n                    gene knocked out (GLA1), with enhanced glucose uptake. In\u00a0vitro and in\u00a0vivo assays were performed to assess tumor cell glucose deprivation, mitochondrial stress, cytosolic mitochondrial DNA (mtDNA) release, and activation of the cGAS\/STING pathway. An engineered strain, GLA2, was generated from the AISIH strain by knockout of the\n                    <jats:italic toggle=\"yes\">glpX<\/jats:italic>\n                    gene and was subsequently further engineered to locally deliver an anti-tumor necrosis factor-\u03b1 (TNF-\u03b1) nanobody under quorum-sensing control. Efficacy was evaluated in subcutaneous and orthotopic bladder cancer models, with analysis of tumor-infiltrating immune cells, dendritic cell (DC) maturation, and T cell priming.\n                    <jats:bold>Results:<\/jats:bold>\n                    GLA1 competitively depleted glucose in the bladder tumor microenvironment, inducing energy stress, mitochondrial damage, and mtDNA release, which noncanonically activated the STING pathway. This promoted type I interferon production, DC maturation, and antitumor immune responses. However, TNF-\u03b1-mediated vascular abnormalities limited efficacy. GLA2 normalized tumor vasculature via local anti-TNF-\u03b1 delivery, enhancing nutrient competition and immune activation. Both strains markedly suppressed tumor growth, with GLA2 showing superior efficacy due to synergistic metabolic and immune reprogramming.\n                    <jats:bold>Conclusions:<\/jats:bold>\n                    This study demonstrates that bacterial competition for glucose is a pivotal mechanism of antitumor activity in bladder cancer, linking metabolic stress to STING-dependent immune activation. Engineered\n                    <jats:italic toggle=\"yes\">Salmonella<\/jats:italic>\n                    strains that combine enhanced glucose uptake with local vascular normalization offer a robust platform for bladder cancer. These findings highlight a novel strategy to integrate microbial metabolic engineering with immune modulation, providing a foundation for precision bacteriotherapy in oncology.\n                  <\/jats:p>","DOI":"10.34133\/cancomm.0060","type":"journal-article","created":{"date-parts":[[2026,9,29]],"date-time":"2026-09-29T13:22:46Z","timestamp":1790688166000},"update-policy":"https:\/\/doi.org\/10.34133\/aaas_crossmark_01","source":"Crossref","is-referenced-by-count":0,"title":["Metabolic Competition-Driven Antitumor Immunity of\n                    <i>glpX<\/i>\n                    -Deficient Engineered\n                    <i>Salmonella<\/i>\n                    via Glucose Deprivation and STING Activation in Bladder Cancer"],"prefix":"10.34133","volume":"46","author":[{"given":"Leyang","family":"Wu","sequence":"first","affiliation":[{"name":"State Key Laboratory of Pharmaceutical Biotechnology, School of Life Sciences, \rNanjing University, Nanjing, Jiangsu, P. R. 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