Frontiers in immunology · 2026
Study of JCAD for prognosis and immune infiltration in hepatocellular carcinoma.
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Wang Zhonghua, Tang Jing, Zhu Siyuan, Li Shan, Yao Bingyue, Tu Jiayi, Zhou Xingyue, Tang Qinghe, Zhong Lan
Аннотация
BACKGROUND: Hepatocellular carcinoma (HCC) remains a common malignant tumor with high morbidity and mortality. Junctional protein associated with coronary artery disease (JCAD), a cell junction-related protein, plays critical roles in multiple pathological processes. However, the prognostic value of JCAD in HCC, particularly its correlation with immune cell infiltration, remains unclear.
METHODS: We comprehensively analyzed the biological characteristics of JCAD in HCC using multiple databases and tools. These included The Cancer Genome Atlas (TCGA), Gene Expression Omnibus (GEO), Genotype-Tissue Expression (GTEx), the KM-Plotter platform, and Xiantao Academic tools. Systematic evaluations were performed to assess its protein expression profile, prognostic value, functional enrichment, and immune cell infiltration. Based on TCGA data, we explored correlations between JCAD expression and immune cell infiltration levels. We also assessed whether the impact of JCAD expression on HCC prognosis is partially mediated through immune infiltration. Furthermore, immunohistochemistry assessed JCAD expression in 102 pairs of human HCC and adjacent normal tissues, followed by analysis of its associations with clinicopathological features and disease-free survival (DFS).
RESULTS: Bioinformatics analysis revealed that patients with high JCAD expression had poorer overall survival and showed correlations with gender, tumor stage, and differentiation grade. Notably, JCAD expression was correlated with immune cell infiltration levels, and its association with HCC survival appeared to be partially mediated through immune-related pathways. Clinical validation confirmed JCAD upregulation in 44.1% of HCC tissues. High JCAD expression was significantly associated with portal vein tumor thrombosis and reduced DFS. Kaplan-Meier analysis showed that patients with high JCAD expression had significantly shorter DFS (log-rank p = 0.0012), with lower 1- and 3-year DFS rates compared to the low-expression group. ROC curve analysis indicated that JCAD has modest predictive power for DFS, with an AUC of 0.695 (0.592-0.798).
CONCLUSION: Elevated JCAD expression may serve as a prognostic biomarker for HCC patients, potentially through immune-related mechanisms. By integrating bioinformatics analysis with clinical validation, this study provides novel evidence supporting the role of JCAD in HCC prognosis and its potential association with immune regulation.
METHODS: We comprehensively analyzed the biological characteristics of JCAD in HCC using multiple databases and tools. These included The Cancer Genome Atlas (TCGA), Gene Expression Omnibus (GEO), Genotype-Tissue Expression (GTEx), the KM-Plotter platform, and Xiantao Academic tools. Systematic evaluations were performed to assess its protein expression profile, prognostic value, functional enrichment, and immune cell infiltration. Based on TCGA data, we explored correlations between JCAD expression and immune cell infiltration levels. We also assessed whether the impact of JCAD expression on HCC prognosis is partially mediated through immune infiltration. Furthermore, immunohistochemistry assessed JCAD expression in 102 pairs of human HCC and adjacent normal tissues, followed by analysis of its associations with clinicopathological features and disease-free survival (DFS).
RESULTS: Bioinformatics analysis revealed that patients with high JCAD expression had poorer overall survival and showed correlations with gender, tumor stage, and differentiation grade. Notably, JCAD expression was correlated with immune cell infiltration levels, and its association with HCC survival appeared to be partially mediated through immune-related pathways. Clinical validation confirmed JCAD upregulation in 44.1% of HCC tissues. High JCAD expression was significantly associated with portal vein tumor thrombosis and reduced DFS. Kaplan-Meier analysis showed that patients with high JCAD expression had significantly shorter DFS (log-rank p = 0.0012), with lower 1- and 3-year DFS rates compared to the low-expression group. ROC curve analysis indicated that JCAD has modest predictive power for DFS, with an AUC of 0.695 (0.592-0.798).
CONCLUSION: Elevated JCAD expression may serve as a prognostic biomarker for HCC patients, potentially through immune-related mechanisms. By integrating bioinformatics analysis with clinical validation, this study provides novel evidence supporting the role of JCAD in HCC prognosis and its potential association with immune regulation.