Published online Mar 28, 2025. doi: 10.3748/wjg.v31.i12.103991
Revised: January 26, 2025
Accepted: February 24, 2025
Published online: March 28, 2025
Processing time: 110 Days and 15.7 Hours
Keratin 80 (KRT80), a type I intermediate filament protein, is a member of the keratin family with specialized functions in epithelial tissues. While KRT80 has been implicated in both normal physiological processes and various diseases, its role in gastric cancer (GC), particularly its expression and prognostic significance, remains poorly understood. In this study, we investigated the role and underlying molecular mechanisms of KRT80 in oxaliplatin resistance in GC. Our analysis revealed that KRT80 is significantly upregulated in GC tissues and is associated with poor clinical prognosis. The role of KRT80 in GC cell proliferation was assessed through in vitro and in vivo assays.
To explore the expression of KRT80 in GC and its impact on the prognosis of pa
KRT80 expression in GC tissues was analyzed using Western blotting, quan
Integrating our experimental findings with multiple published studies, we found that increased KRT80 expression is associated with poor prognosis in GC and promotes resistance to oxaliplatin. Moreover, we have preliminarily verified the interaction between KRT80 and EEF1A1. Therefore, this study provides a novel perspective on overcoming oxaliplatin resistance in GC.
Increased KRT80 expression predicts poor prognosis and promotes oxaliplatin resistance in GC, suggesting its potential as a novel prognostic biomarker.
Core Tip: In this paper, keratin 80 (KRT80) was found to be overexpressed in gastric cancer (GC) tissues, functioning as an oncogene and correlating with poor patient prognosis. KRT80 promoted GC proliferation, migration, invasion abilities and oxaliplatin resistance by activating the NF-κB signaling pathway. Immunoprecipitation and mass spectrometry analyses identified elongation factor 1-alpha 1 (EEF1A1) as a binding protein of KRT80, enhancing its protein stability. Notably, knockdown of EEF1A1 partially reversed the effects of KRT80 overexpression in GC cells.