eIF6: a promising therapeutic target for gastric carcinoma via PI3K/AKT pathway modulation.

Background: Gastric carcinoma (GC) is a leading cause of cancer-related deaths, with a dire prognosis for advanced stages. The molecular mechanisms underlying GC progression are not fully understood, necessitating research into novel biomarkers and therapeutic targets. This study investigates the role of eukaryotic translation initiation factor 6 (eIF6) in GC, focusing on its potential as a prognostic indicator and its impact on tumor biology.

Methods: We analyzed eIF6 expression in GC tissues using data from TCGA and GEO databases. Experiments included western blot, IHC staining, and cell culture assays on GC cell lines to evaluate the effect of eIF6 on cell proliferation, invasion, and apoptosis. Statistical analyses were performed using Student's t-tests and ANOVA, with significance set at p < 0.05.

Results: eIF6 was found to be significantly overexpressed in GC tissues, associated with advanced tumor stage and poor patient survival. Functional assays demonstrated that eIF6 knockdown inhibits GC cell proliferation and invasion while promoting apoptosis. Transcriptomic analysis linked eIF6 to the PI3K/AKT pathway, a critical regulator in cancer.

Conclusions: eIF6's overexpression in GC suggests its role in tumor progression, highlighting its potential as a therapeutic target. The study provides a foundation for developing targeted therapies against eIF6 and emphasizes the need for further research into its regulatory mechanisms in GC.