Development and validation of a selenium metabolism regulators associated prognostic model for hepatocellular carcinoma

BackgroundSelenium metabolism has been implicated in human health. This study aimed to identify a selenium metabolism regulator-based prognostic signature for hepatocellular carcinoma (HCC) and validate the role of INMT in HCC.MethodsTranscriptome sequencing data and clinical information related to selenium metabolism regulators in TCGA liver cancer dataset were analysed. Next, a selenium metabolism model was constructed by multiple machine learning algorithms, including univariate, least absolute shrinkage and selection operator, and multivariate Cox regression analyses. Then, the potential of this model for predicting the immune landscape of different risk groups was evaluated. Finally, INMT expression was examined in different datasets. After knockdown of INMT, cell proliferation and colony formation assays were conducted.ResultsA selenium metabolism model containing INMT and SEPSECS was established and shown to be an independent predictor of prognosis. The survival time of low-risk patients was significantly longer than that of high-risk patients. These two groups had different immune environments. In different datasets, including TCGA, GEO, and our PUMCH dataset, INMT was significantly downregulated in HCC tissues. Moreover, knockdown of INMT significantly promoted HCC cell proliferation.ConclusionsThe current study established a risk signature of selenium metabolism regulators for predicting the prognosis of HCC patients. INMT was identified as a biomarker for poor prognosis of HCC.

Automated summary

The study established a prognostic biomarker based on selenium metabolism regulators for hepatocellular carcinoma (HCC) and validated the role of INMT in HCC. A selenium metabolism model containing INMT and SEPSECS was constructed, which was shown to be an independent predictor of prognosis. The low-risk group had significantly longer survival time compared to the high-risk group, and these two groups exhibited different immune environments. INMT was significantly downregulated in HCC tissues in different datasets, and knockdown of INMT promoted HCC cell proliferation.