Chinese clinical oncology · 2026
Fos-related antigen 1 is required for Helicobacter pylori-induced inflammatory response in gastric epithelial cells through NF-κB pathway.
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Yang Yang, Shao Shihe
Аннотация
BACKGROUND: Chronic gastritis affects ~50% of the population, frequently linked to Helicobacter pylori (H. pylori). Fos-related antigen 1 (FRA-1) has been reported to be involved in stomach inflammation and malignancy. The study aimed to investigate the regulatory role of FRA-1 in H. pylori-induced inflammatory response of gastric epithelial cells, and to explore its mechanism and application prospect of FRA-1 in H. pylori infection treatment.
METHODS: GES-1 cells were selected to knock down the level of FRA-1 by specific small interfering RNA (siRNA) prior to H. pylori infection. The messenger RNA (mRNA) expression of FRA-1 and cytokines was quantified by real-time quantitative polymerase chain reaction (RT-qPCR), protein levels were analyzed by western blot, and cytokine secretion was measured by enzyme-linked immunosorbent assay (ELISA). Nuclear factor-κB (NF-κB) activity was then assessed by western blot and immunofluorescence.
RESULTS: It was showed that infection with H. pylori markedly increased FRA-1 expression levels. Knockdown analysis identified that FRA-1 was required for H. pylori-induced inflammatory cytokines expression in GES-1 cells. In addition, FRA-1 exerted proinflammatory response to H. pylori by augmenting NF-κB activation.
CONCLUSIONS: This work suggests a key function for FRA-1 in underlying the inflammatory pathology of H. pylori-associated gastritis, and that it could serve as a useful detection indicator and therapeutic target.
METHODS: GES-1 cells were selected to knock down the level of FRA-1 by specific small interfering RNA (siRNA) prior to H. pylori infection. The messenger RNA (mRNA) expression of FRA-1 and cytokines was quantified by real-time quantitative polymerase chain reaction (RT-qPCR), protein levels were analyzed by western blot, and cytokine secretion was measured by enzyme-linked immunosorbent assay (ELISA). Nuclear factor-κB (NF-κB) activity was then assessed by western blot and immunofluorescence.
RESULTS: It was showed that infection with H. pylori markedly increased FRA-1 expression levels. Knockdown analysis identified that FRA-1 was required for H. pylori-induced inflammatory cytokines expression in GES-1 cells. In addition, FRA-1 exerted proinflammatory response to H. pylori by augmenting NF-κB activation.
CONCLUSIONS: This work suggests a key function for FRA-1 in underlying the inflammatory pathology of H. pylori-associated gastritis, and that it could serve as a useful detection indicator and therapeutic target.