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

BACKGROUND

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

AIM

To explore the role and mechanism of in the pathogenesis of () infection.

METHODS

GES-1 was co-cultured with to detect changes in the expression of . Overexpression and silencing of were performed. Quantitative real-time polymerase chain reaction (q-PCR) and Western blot (WB) were used to determine mRNA and protein expression of , protein kinase B (AKT)/mammalian target of rapamycin (mTOR), and epithelial-mesenchymal transition-related factors and ; 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 expression in cancer tissues.

RESULTS

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

CONCLUSION

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