ArticleJournal of applied genetics2025
Exploring the pathogenic mechanism of RNH1 in colorectal cancer based on eQTL, Multi-omics and deep learning.
Article in Journal of applied genetics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundColorectal cancer (CRC) is a major global health concern with increasing incidence. Current treatments, though improved, require novel biomarkers for better diagnosis and management. Disulfidptosis, a recently characterized form of cell death, may play a critical role in CRC progression.
methodsUtilizing summary-data-based Mendelian randomization (SMR), we identified RNH1 as a gene linked to CRC and disulfidptosis. The expression and intercellular communication of RNH1 in CRC were analyzed using single-cell RNA sequencing (scRNA-seq) and spatial transcriptome sequencing (stRNA-seq). A prognostic model was built using a Deep Learning Survival Neural Network (DeepSurv). Additionally, we performed RNA sequencing (RNA-seq) analysis to analyze the function of RNH1. Validation was performed through qPCR on CRC and normal tissue samples.
resultsRNH1 was identified as a gene linked to disulfidptosis and positively correlated with CRC risk. scRNA-seq analysis revealed that RNH1 + malignant cells showed distinct metabolic pathways and greater cell interactions. stRNA-seq analysis confirmed these interactions, especially with endothelial cells. DeepSurv analysis produced a prognostic model, showing different survival outcomes between high-risk and low-risk groups. RNA-seq analysis showed that the RNH1 + high expression group had higher immune cell abundance scores and tumor microenvironment scores, and RNH1 was positively correlated with most immune checkpoints. Drug sensitivity analysis suggested that CRC patients with high RNH1 expression were more sensitive to certain therapeutic agents. qPCR showed that the expression level of RNH1 in cancer tissues of CRC patients was significantly higher than that in normal tissues.
conclusionRNH1 acts as a biomarker for CRC, influencing tumor growth via disulfidptosis, tumor microenvironment alterations, and metabolic pathways. Its high expression correlates with immune escape. This study suggests RNH1 as a potential therapeutic target for CRC, warranting further exploration of its mechanistic roles and treatment potential.
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