Epithelial <i>Ikkβ</i> deletion modulates immune responses and the IFNγ/CXCL9 axis during early esophageal carcinogenesis.

ABSTRACT: Esophageal cancer is a major cause of cancer-related death, often preceded with chronic inflammation and injuries. The NFκB/IKKβ pathway plays a central role in inflammation, yet its role in early esophageal carcinogenesis remains unclear. This study investigated the role of epithelial IKKβ in early esophageal carcinogenesis. Mice were treated with the carcinogen 4-nitroquinoline-1-oxide (4-NQO) or a vehicle for one month to induce precancerous lesions. Esophagi were harvested and examined through histological, protein, flow cytometry, and RNA analyses. Histological analysis revealed that 4-NQO treatment led to increased inflammation, intraepithelial CD45+ immune cells, and elevated IKKβ phosphorylation levels. Mice with esophageal epithelial-specific Ikkβ deletion (4-NQO/Ikkβ

SUBMITTER: Hodge N 

PROVIDER: S-EPMC11957055 | biostudies-literature | 2025 Mar

REPOSITORIES: biostudies-literature