ArticleJournal of cellular and molecular medicine2024
Integrated Single-Cell and Spatial Transcriptome Reveal Metabolic Gene SLC16A3 as a Key Regulator of Immune Suppression in Hepatocellular Carcinoma.
Article in Journal of cellular and molecular medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- SLC16A3 links tumor metabolism to therapeutic opportunities in hepatocellular carcinoma.Translational cancer research · 2026Review
- Review
- Lactate metabolism-related interaction perturbation network enables robust stratification of hepatocellular carcinoma.Discover oncology · 2026Article
- Redox-driven mitochondrial DNA stress in hepatocellular carcinoma: innate immune remodelling, tumour immune escape, and immunotherapy implications.Frontiers in immunology · 2026Review
- A Prognostic Risk Model for Hepatocellular Carcinoma Integrating Ferroptosis and Metabolic Reprogramming Signatures.Journal of Cancer · 2026Article
- SLC16A3 as an immunosuppressive Kupffer cell marker predicts poor prognosis in HBV-positive hepatocellular carcinoma.Journal of translational medicine · 2025Article
- Targeting Lactylation: From Metabolic Reprogramming to Precision Therapeutics in Liver Diseases.Biomolecules · 2025Review
- SLC16A3 drives lung adenocarcinoma progression and gefitinib resistance through coordinated regulation of ferroptosis and lactate metabolism.Frontiers in immunology · 2025Article
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
Hepatocellular carcinoma (HCC) is one of the most lethal cancers, usually diagnosed at an advanced stage. Metabolic reprogramming plays a significant role in HCC progression, probably related to immune evasion, yet the key gene is unclear. In this study, six metabolism-related genes with prognostic implications were screened. Correlation analysis between the key genes and immune cell subtypes was conducted, and a prominent gene strongly associated with immunosuppression, SLC16A3, was identified. Overexpression of SLC16A3 is associated with the loss of T-cell function and might lead to the upregulation of several immunosuppressive proteins. Gene function enrichment analysis showed genes correlated with SLC16A3 primarily involved in cell adhesion. Single-cell analysis showed that the SLC16A3 gene was mainly expressed in macrophages, especially some tumour-promoting macrophages. Further analysis of spatial transcriptome data indicated that SLC16A3 was enriched at the tumour invasion front. The mIHC revealed that patients with high SLC16A3 expression exhibited significantly reduced infiltration of GZMB
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