Helicobacter pylori CagA elevates FTO to induce gastric cancer progression via a "hit-and-run" paradigm.

ABSTRACT:

Background

Helicobacter pylori (H. pylori) infection contributes significantly to gastric cancer (GC) progression. The intrinsic mechanisms of H. pylori-host interactions and their role in promoting GC progression need further investigation. In this study, we explored the potential role of fat mass and obesity-associated protein (FTO) in mediating Cytotoxin-associated gene A (CagA)-induced GC progression.

Methods

The effects of H. pylori infection on N⁶-methyladenosine (m⁶A) modification were evaluated in both human samples and GC cell lines. The function of FTO in the progression of GC was elucidated through in vitro and in vivo studies. A series of techniques, including methylated RNA immunoprecipitation sequencing, RNA sequencing, RNA binding protein

SUBMITTER: He B 

PROVIDER: S-EPMC12067399 | biostudies-literature | 2025 May

REPOSITORIES: biostudies-literature