DOI: 10.57760/sciencedb.j00217.11088
title: The Role of SLC25A1 in Immune Infiltration and OXPHOS Metabolism of Hepatocellular Carcinoma Explored by Metabolomic and Transcriptomic Sequencing
title: 基于代谢组和转录组测序探索SLC25A1与肝细胞癌的免疫浸润及氧化磷酸化代谢的关系

description: Methods Firstly, we utilized the TIMER2.0, UALCAN, SangerBox, cBioPortal, GeneMANIA, and TNM Plot databases to explore the mRNA expression, prognosis, clinical features, immune infiltration, and correlation with OXPHOS of SLC25A1 in LIHC. Explore the effect of SLC25A1 on the proliferation of liver cancer cells through CCK-8 experiments and clone formation experiments. Subsequently, Gene Set Enrichment Analysis (GSEA) was performed to identify the main functions of SLC25A1. Finally, we analyzed the biological processes associated with SLC25A1 and LIHC through metabolomics sequencing and transcriptomics measurement.Results The mRNA expression level of SLC25A1 was significantly higher in LIHC tissues compared to normal tissues, and its high expression was correlated with advanced clinical stage and poor prognosis in LIHC patients. The CCK-8 experiment and clone formation experiment showed that inhibiting SLC25A1 significantly affected the proliferation of liver cancer cells. GSEA revealed that SLC25A1 was involved in mitochondrial-related signaling pathways and was closely associated with the mitochondrial OXPHOS metabolic pathway in LIHC. SangerBox analysis revealed that SLC25A1 was associated with immune infiltration, immune checkpoints, and immune cells. Metabolomics sequencing and transcriptomics sequencing demonstrated that inhibition of SLC25A1 significantly inhibited mitochondrial OXPHOS metabolism in LIHC. It is worth noting that UQCRB has a significant interaction among the intersecting genes significantly affected by SLC25A1 inhibition.Conclusion SLC25A1 may serve as a prognostic biomarker and a potential target for personalized therapy in LIHC.Obstract To investigate the expression of solute carrier family 25 member 1 (SLC25A1) in hepatocellular carcinoma and analyze its correlation with patient prognosis, clinical stage, immune infiltration, and oxidative phosphorylation metabolism.
description: Methods Firstly, we utilized the TIMER2.0, UALCAN, SangerBox, cBioPortal, GeneMANIA, and TNM Plot databases to explore the mRNA expression, prognosis, clinical features, immune infiltration, and correlation with OXPHOS of SLC25A1 in LIHC. Explore the effect of SLC25A1 on the proliferation of liver cancer cells through CCK-8 experiments and clone formation experiments. Subsequently, Gene Set Enrichment Analysis (GSEA) was performed to identify the main functions of SLC25A1. Finally, we analyzed the biological processes associated with SLC25A1 and LIHC through metabolomics sequencing and transcriptomics measurement.Results The mRNA expression level of SLC25A1 was significantly higher in LIHC tissues compared to normal tissues, and its high expression was correlated with advanced clinical stage and poor prognosis in LIHC patients. The CCK-8 experiment and clone formation experiment showed that inhibiting SLC25A1 significantly affected the proliferation of liver cancer cells. GSEA revealed that SLC25A1 was involved in mitochondrial-related signaling pathways and was closely associated with the mitochondrial OXPHOS metabolic pathway in LIHC. SangerBox analysis revealed that SLC25A1 was associated with immune infiltration, immune checkpoints, and immune cells. Metabolomics sequencing and transcriptomics sequencing demonstrated that inhibition of SLC25A1 significantly inhibited mitochondrial OXPHOS metabolism in LIHC. It is worth noting that UQCRB has a significant interaction among the intersecting genes significantly affected by SLC25A1 inhibition.Conclusion SLC25A1 may serve as a prognostic biomarker and a potential target for personalized therapy in LIHC.Obstract To investigate the expression of solute carrier family 25 member 1 (SLC25A1) in hepatocellular carcinoma and analyze its correlation with patient prognosis, clinical stage, immune infiltration, and oxidative phosphorylation metabolism.