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Oxidative stress (OS) is a crucial factor promoting the progression of liver hepatocellular carcinoma (LIHC). This study was designed to develop an OS-based RiskScore model.
Publicly available RNA-seq data and clinical data of LIHC patients, as well as an OS-related gene set, were collected. The differentially expressed genes (DEGs) were calculated, and functional enrichment analysis was performed. Then, a RiskScore model was established, and Kaplan-Meier survival and receiver operating characteristic analyses were performed. Immune infiltration was analyzed, and tumor cell migration and invasion were detected.
4,118 DEGs were identified in the TCGA-LIHC cohort, while 1,632 DEGs were recognized in the ICGC cohort. The upregulated DEGs were closely related to the cell cycle pathway, while the downregulated DEGs were linked to the metabolic pathway. A 4-gene RiskScore model accurately divided patients into high- and low-risk groups, showing strong classification effectiveness. Patients in the high-risk group exhibited worse prognosis, elevated TIDE scores, frequent p53 mutations, and higher immune cell infiltration. In vitro experiments confirmed that these model genes were overexpressed in tumor cells as risk factors, with SPP1 notably influencing tumor cell migration and invasion. Furthermore, by combining the RiskScore with other clinical features, we developed a nomogram that precisely guides survival assessment in LIHC. Finally, the association of RiskScore with OS and multiple metabolic pathways was noticed.
This study proposes a novel RiskScore model for LIHC based on the OS feature, which still requires further verification.
We establish an OS-related risk model to guide the treatment of LIHC.
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