• Gang Chen, Zhipeng Du, and Caijun Rao.
• Department of Geriatrics, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
• Int J Med Sci. 2024 Jan 1; 21 (15): 306930823069-3082.

AbstractSolute carrier 41 (SLC41) has been identified as a family of magnesium (Mg2+) transporters that participate in various diseases, including tumor development and progression. Recent studies revealed SLC41A3 acted as an oncogene and predicted poor survival for hepatocellular carcinoma (HCC) patients. However, the potential function of SLC41A1 in HCC remains unclear. In our study, we focused on the levels and putative mechanisms of SLC41A1 in HCC. Using bioinformatics techniques, we found SLC41A1 was upregulated in HCC, which was verified by immunostaining of HCC patients. SLC41A1 was correlated with clinicopathological characteristics, and could be utilized as independently diagnostic and prognostic markers for HCC. By exploring MethSurv website, DNA methylation was identified in SLC41A1, and several methylated CpG sites might affect overall survival of HCC patients. Using Gene Ontology (GO) , Kyoto Encyclopedia of Genes and Genomes (KEGG), gene set enrichment analysis (GSEA), protein-protein interaction (PPI) network, we found SLC41A1 overexpression was related to several tumor-promoting pathways and molecules, such as degradation of extracellular matrix, cell adhesion and O-linked glycosylation, and expression of CXCL1, CXCL5 and MUC1. The results of single-sample GSEA (ssGSEA) showed SLC41A1 might regulate infiltration of multiple immune cells, resulting in the imbalance between immune suppression and immune surveillance. Cellular experiments showed that knockdown of SLC41A1 inhibited proliferation, migration and invasion of HCC, whereas SLC41A1 overexpression exerted the tumor-promoting effects. Collectively, our results shed light on new insights into expression, putative roles and mechanisms of SLC41A1 in HCC, providing novel diagnostic biomarkers and therapeutic targets for HCC.© The author(s).

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