ObjectiveTRIM25 has been reported to promote hepatocellular carcinoma (HCC) cell survival by activating the Keap1-Nrf2 pathway. However, its expression profile in clinical HCC specimens and its potential role in regulating ferroptosis remain to be elucidated.
This study aimed to determine the expression pattern of TRIM25 in primary HCC and its association with clinicopathological features and prognosis, utilizing both bioinformatic analysis and experimental validation in clinical samples and cell lines. In parallel, we investigated the regulatory effect of TRIM25 on ferroptosis in HCC cells, thereby offering experimental insights that could inform prognosis assessment and the development of targeted therapies for HCC.MethodsTo investigate the expression pattern of TRIM25 in hepatocellular carcinoma and its clinical relevance, we obtained RNA-seq data and corresponding clinical staging information from The Cancer Genome Atlas.
After data normalization, the Kruskal–Wallis H test was applied to assess TRIM25 expression differences across tumor stages. Transcriptomic data were also retrieved from the International Cancer Genome Consortium, and following normalization, the Wilcoxon rank-sum test was used to compare TRIM25 expression between HCC tumors and matched adjacent non-tumor tissues.
Frontiers in Immunology published a clinical update in Infectious Disease on 01 Apr 2026.
The item focuses on TRIM25-mediated ferroptosis resistance is closely associated with poor prognosis in hepatocellular carcinoma.
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