Transcriptomic Analysis Reveals the Role of TRIM26 in Hepatocellular Carcinoma and Its Association With the Wnt/β-catenin Signaling Pathway.
Hepatocellular carcinoma (HCC) shows high incidence and mortality worldwide. TRIM26, an E3 ubiquitin ligase within the TRIM family, exerts regulatory functions in various tumors. This study analyzed the expression patterns and potential functions of TRIM26 in HCC based on transcriptomic data.
First, the differential expression of TRIM26 between tumor and normal tissues was analyzed using the TCGA dataset and cross-validated using TIMER 2.0 and HCCDB. Enrichment analysis evaluated its association with hallmark pathways including Wnt/β-catenin. A gene functional interaction network was built via GeneMANIA to explore TRIM26 and the Wnt/β-catenin pathway. Immune cell infiltration was quantified by ssGSEA for immune microenvironment correlation. scRNA-seq data established an HCC single-cell atlas to define TRIM26 distribution across cell subsets. AUCell was used to assess TRIM26-pathway associations within specific cell types.
TRIM26 was significantly upregulated in HCC tissues, and its high expression correlated with enrichment of oncogenic pathways including Wnt/β-catenin, G2/M checkpoint, and TGF-β. GeneMANIA showed that TRIM26 interacted directly or indirectly with Wnt/β-catenin core molecules, implying its regulatory role. TRIM26 expression was closely linked to infiltration of activated B cells, CD8+ T cells, and NKT cells. Single-cell analysis revealed TRIM26 was mainly expressed in hepatocytes, T/NK cells, myeloid cells, and B cells. Importantly, in hepatocytes, TRIM26 strongly correlated with Wnt/β-catenin activity, which was much higher in tumor hepatocytes than normal ones.
In HCC, TRIM26 was abnormally overexpressed. TRIM26 may regulate tumor progression via the Wnt/β-catenin pathway and is linked to immune infiltration. Thus, TRIM26 is a potential therapeutic target for HCC.
First, the differential expression of TRIM26 between tumor and normal tissues was analyzed using the TCGA dataset and cross-validated using TIMER 2.0 and HCCDB. Enrichment analysis evaluated its association with hallmark pathways including Wnt/β-catenin. A gene functional interaction network was built via GeneMANIA to explore TRIM26 and the Wnt/β-catenin pathway. Immune cell infiltration was quantified by ssGSEA for immune microenvironment correlation. scRNA-seq data established an HCC single-cell atlas to define TRIM26 distribution across cell subsets. AUCell was used to assess TRIM26-pathway associations within specific cell types.
TRIM26 was significantly upregulated in HCC tissues, and its high expression correlated with enrichment of oncogenic pathways including Wnt/β-catenin, G2/M checkpoint, and TGF-β. GeneMANIA showed that TRIM26 interacted directly or indirectly with Wnt/β-catenin core molecules, implying its regulatory role. TRIM26 expression was closely linked to infiltration of activated B cells, CD8+ T cells, and NKT cells. Single-cell analysis revealed TRIM26 was mainly expressed in hepatocytes, T/NK cells, myeloid cells, and B cells. Importantly, in hepatocytes, TRIM26 strongly correlated with Wnt/β-catenin activity, which was much higher in tumor hepatocytes than normal ones.
In HCC, TRIM26 was abnormally overexpressed. TRIM26 may regulate tumor progression via the Wnt/β-catenin pathway and is linked to immune infiltration. Thus, TRIM26 is a potential therapeutic target for HCC.