Helicobacter pylori reduces METTL14-mediated VAMP3 m⁶A modification and promotes the development of gastric cancer by regulating LC3C-mediated c-Met recycling.

ABSTRACT: Helicobacter pylori (H. pylori) plays an important role in the malignant transformation of the gastric mucosa from chronic inflammation to cancer. However, the mechanisms underlying the epigenetic regulation of gastric carcinogenesis mediated by H. pylori remain unclear. Here, we uncover that H. pylori inhibits METTL14 by upregulating ATF3. METTL14 inhibits gastric cancer (GC) cell proliferation and metastasis in vitro and in vivo. Downregulation of METTL14 inhibits Vesicle-associated membrane protein-3 (VAMP3) by reducing the m⁶A modification level of VAMP3 mRNA and the stability of IGF2BP2-dependent mRNA. H. pylori also accelerates the malignant progression of GC by regulating VAMP3/LC3C-mediated c-Met recycling. Moreover, the expression of METTL14 and VAMP3 in Hp+ chronic gas

SUBMITTER: Cui X 

PROVIDER: S-EPMC11742886 | biostudies-literature | 2025 Jan

REPOSITORIES: biostudies-literature