March 3, 2026Open Access

Tumor neoantigen gene C7orf50 remodels the immune microenvironment by recruiting tumor-associated macrophages to promote hepatocellular carcinoma progression and lung metastasis

Key Points

C7orf50 mediates the immune microenvironment remodeling, promoting HCC progression and lung metastasis, and indicates potential for targeted therapies.
High expression levels of C7orf50, PAI-1, and CD68 serve as independent prognostic markers for HCC outcomes.
This analysis examines molecular pathways, focusing on the NF-κB/PAI-1 pathway and its role in tumor-associated macrophage recruitment.
Findings underscore the potential of C7orf50-related neoantigens in precision medicine and immunotherapy for HCC, paving the way for further research.

Abstract

C7orf50 is a critical mediator of HCC progression and lung metastasis, acting through the NF-κB/PAI-1 pathway and AEG-1. Its expression levels, along with those of PAI-1 and CD68, serve as independent prognostic markers. And C7orf50-related neoantigen shows great application potential in TCR-T therapy. These findings provide a foundation for developing C7orf50-targeted therapies and highlight its potential in precision medicine and immunotherapy for HCC.

Tumor neoantigen gene C7orf50 remodels the immune microenvironment by recruiting tumor-associated macrophages to promote hepatocellular carcinoma progression and lung metastasis

Key Points

Abstract

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