IL-17A promotes Helicobacter pylori-induced gastric carcinogenesis via interactions with IL-17RC.

ABSTRACT:

Background

Gastric cancer (GC) is a common malignancy worldwide, with a major attribution to Helicobacter pylori. Interleukin (IL)-17A has been reported to be up-regulated in serum and tumor of GC patients, but the precise mechanisms underlying its involvement in gastric tumorigenesis are yet to be established. Here, we investigated the roles of IL-17A in the pathogenesis of H. pylori-induced GC.

Methods

GC was induced in IL-17A knockout (KO) and wild-type (WT) mice via N-methyl-N-nitrosourea (MNU) treatment and H. pylori infection. At 50 weeks after treatment, gastric tissues were examined by histopathology, immunohistochemistry, and immunoblot analyses. In vitro experiments on the human GC cell lines were additionally performed to elucidate the underlying mechanisms.

Re

SUBMITTER: Kang JH 

PROVIDER: S-EPMC9813207 | biostudies-literature | 2023 Jan

REPOSITORIES: biostudies-literature