RPF2 regulates the protein kinase B/mammalian target of rapamycin pathway in the pathogenesis of Helicobacter pylori.

Abstract

Background: RPF2 is a crucial factor in ribosome synthesis, which has been linked to the development of several cancers. However, the mechanism of RPF2 in gastric carcinogenesis is unclear.

Aim: To explore the role and mechanism of RPF2 in the pathogenesis of Helicobacter pylori (H. pylori) infection.

Methods: GES-1 was co-cultured with H. pylori in vitro to detect changes in the expression of RPF2. Overexpression and silencing of RPF2 were performed. Quantitative real-time polymerase chain reaction (q-PCR) and Western blot (WB) were used to determine mRNA and protein expression of RPF2, protein kinase B (AKT)/mammalian target of rapamycin (mTOR), and epithelial-mesenchymal transition-related factors MMP2 and MMP9; cell counting kit 8 and wound healing assays were utilized to evaluate cell viability and migratory capacity; q-PCR, WB, and immunohistochemistry were employed to establish RPF2 expression in cancer tissues.

Results: H. pylori facilitated RPF2 expression and triggered AKT/mTOR signaling pathway. Functional experiments showed that RPF2 overexpression could promote a series of malignant transformations such as cell proliferation, cell migration and invasion, and further enhance AKT/mTOR signaling pathway activation. RPF2 knockdown had the opposite effect. In addition, RPF2 expression was higher in gastric cancer tissues than in adjacent tissues.

Conclusion: RPF2 plays a significant role in the pathogenic mechanism of H. pylori infection and may be useful in the detection and management of gastric cancer caused by H. pylori infection.