Journal
CANCER LETTERS
Volume 530, Issue -, Pages 59-67Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.canlet.2022.01.014
Keywords
Fusobacterium nucleatum; Esophageal cancer; NOD1; RIPK2; NF-kappa B
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Funding
- JSPS KAKENHI [17H04273, 17K19702, 17KK0195]
- Center for Metabolic Regulation of Healthy Aging
- Okukubo Memorial Fund for Medical Research at Kumamoto University School of Medicine
- Grants-in-Aid for Scientific Research [17KK0195, 17K19702, 17H04273] Funding Source: KAKEN
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Fusobacterium nucleatum influences the progression of gastrointestinal cancers by invading and occupying cancer cells, impacting gene and protein expression, and activating signaling pathways. This study provides insights into the mechanism of ESCC progression induced by F. nucleatum.
Fusobacterium nucleatum, found in the oral cavity, influences the progression of gastrointestinal cancers. Addi-tionally, our previous results suggested that F. nucleatum is associated with poor patient prognosis in esophageal squamous cell carcinoma (ESCC). However, the mechanism by which F. nucleatum affects aggressive tumor behavior has yet to be elucidated. We have conducted this clinical, in vitro, and in vivo study to clarify the mechanism of ESCC progression induced by F. nucleatum. Transmission electron microscopy revealed that F. nucleatum invaded and occupied ESCC cells and impacted gene and protein expression. Comprehensive mRNA expression and pathway enrichment analyses of F. nucleatum-treated ESCC cells identified the NF-kappa B and NOD-like receptor signaling pathways as enriched. We confirmed the relationship between the presence of F. nucleatum and NF-kappa B activation in resected ESCC tissues. Furthermore, F. nucleatum-treated ESCC cells demonstrated enhanced growth ability, and NF-kappa B acti-vation, as well as overexpression of NOD1 and phosphorylated RIPK2. Furthermore, treated cells showed accelerated tumor growth, with NF-kappa B activation in xenograft models. F. nucleatum invaded ESCC cells and induced the NF-kappa B pathway through the NOD1/RIPK2 pathway, leading to tumor progression.
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