Seven oxidative stress-related genes predict the prognosis of hepatocellular carcinoma

Abstract

Predicting the prognosis of hepatocellular carcinoma (HCC) is a major medical challenge and of guiding significance for treatment. This study explored the actual relevance of RNA expression in predicting HCC prognosis. Cox's multiple regression was used to establish a risk score staging classification and to predict the HCC patients' prognosis on the basis of data in the Cancer Genome Atlas (TCGA). We screened seven gene biomarkers related to the prognosis of HCC from the perspective of oxidative stress, including Alpha-Enolase 1(ENO1), N-myc downstream-regulated gene 1 (NDRG1), nucleophosmin (NPM1), metallothionein-3, H2A histone family member X, Thioredoxin reductase 1 (TXNRD1) and interleukin 33 (IL-33). Among them we measured the expression of ENO1, NGDP1, NPM1, TXNRD1 and IL-33 to investigate the reliability of the multiindex prediction. The first four markers' expressions increased successively in the paracellular tissues, the hepatocellular carcinoma samples (from patients with better prognosis) and the hepatocellular carcinoma samples (from patients with poor prognosis), while IL-33 showed the opposite trend. The seven genes increased the sensitivity and specificity of the predictive model, resulting in a significant increase in overall confidence. Compared with the patients with higher-risk scores, the survival rates with lower-risk scores are significantly increased. Risk score is more accurate in predicting the prognosis HCC patients than other clinical factors. In conclusion, we use the Cox regression model to identify seven oxidative stress-related genes, investigate the reliability of the multi-index prediction, and develop a risk staging model for predicting the prognosis of HCC patients and guiding precise treatment strategy.

Comprehensive assessment of regulatory T-cells-related scoring system for predicting the prognosis, immune microenvironment and therapeutic response in hepatocellular carcinoma

“…Previous studies have shown that TPP1 is associated with macrophages in HCC [ 34 ], suggesting that there may be a crosstalk of TPP1 between different immune cells. ENO1, which is second only to TPP1 in terms of coefficient in the scoring system, has been shown to promote hepatocarcinogenesis through YAP1-dependent arachidonic acid metabolism and has been implicated in HCC in relation to oxidative stress [ 35 , 36 ]. Additionally, PTTG1 can promote HCC evolution through reprogramming of asparagine metabolism and is a potential therapeutic and diagnostic target for HCC [ 37 ].…”