FBJ MURINE OSTEOSARCOMA VIRAL ONCOGENE HOMOLOG EXPRESSION IN COLON ADENOCARCINOMA: INSIGHTS INTO PATHOGENESIS AND CLINICAL IMPLICATIONS
Main Article Content
Keywords
Colon adenocarcinoma, Diagnosis, Treatment
Abstract
The study focuses on understanding the role of FBJ murine osteosarcoma viral oncogene homolog (FOS) expression and its regulatory mechanisms in colon adenocarcinoma (COAD). Analysis of FOS expression using the UALCAN dataset revealed a consistent down-regulation in cancerous cells compared to normal controls. Further exploration of FOS expression across various clinical parameters demonstrated significant down-regulation across different cancer stages, racial groups, genders, and age groups among COAD patients, suggesting its crucial role in tumor development. Validation of FOS expression using the GEPIA2.0 dataset confirmed its low expression in COAD tumors compared to normal samples. Additionally, validation analysis of FOS expression across different cancer stages showed dysregulation in all stages, with the highest expression in stage I and the lowest in stage IV. The study also investigated the promoter methylation level of FOS, revealing distinct methylation patterns across cancer stages, race groups, genders, and age groups, highlighting its association with COAD pathogenesis. Survival analysis using the KM plotter tool indicated a significant correlation between FOS expression levels and overall and disease-free survival (OS and RFS) in COAD patients, with lower FOS expression not associated with shorter survival times. Mutational analysis using the cBioPortal platform did not reveal any common alterations in COAD samples. These findings underscore the intricate role of FOS in COAD development, emphasizing its potential as a prognostic biomarker and therapeutic target in COAD management.
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