ArticleMolecular medicine (Cambridge, Mass.)2025
DLAT activates EMT to promote HCC metastasis by regulating GLUT1-mediated aerobic glycolysis.
Article in Molecular medicine (Cambridge, Mass.), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed.
- DIXDC1 Promotes Lymphatic Metastasis and Resistance to Cuproptosis in Bladder Cancer Through Mediating DLAT.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Glucose Transporter 1 in Health and Disease.MedComm · 2026Review
- Enhancing pulp regeneration through metabolic reprogramming of mature dental pulp stem cells mediated by GLUT1/HK2 mRNA delivery.International journal of oral science · 2026Article
- Role of KCNQ1OT1 / miR-27b-5p in Modulating Dihydrolipoamide S-acetyltransferase (DLAT): Insights into Cuproptosis in Hepatocellular carcinoma.Biological trace element research · 2026Article
- Hepatocellular carcinoma metastasis-immune microenvironment crosstalk: emerging mechanisms and immunotherapy.Cellular & molecular biology letters · 2026Review
- Glycolytic reprogramming in endometriosis: molecular mechanisms, immune modulation, and non-hormonal therapeutic opportunities.BMC women's health · 2026Review
- Suppression of Tumor Aggression Through Metabolic Reprogramming via Oxamate Targeting LDHA.International journal of molecular sciences · 2026Review
- Metabolic reprogramming in cancer: dysregulation of glucose, lipid, and amino acid pathways and therapeutic opportunities.Molecular biomedicine · 2026Review
- Combinatorial treatment with donafenib and quercetin suppresses lipid metabolism in HepG2 cells by targeting the CREB1/DRP1/SREBP1 axis.Translational cancer research · 2026Article
- Mechanisms of lactylation modification in hepatocellular carcinoma treatment resistance.Gastroenterology report · 2026Review
- DNER drives glycolytic reprogramming in renal cell carcinoma by activating the JAK2/STAT3 signaling pathway.Frontiers in immunology · 2026Article
- Cuproptosis-triggering nanomedicine boosts antitumor immunotherapy.Theranostics · 2026Review
- Molecular regulatory network of glycolytic reprogramming in hepatocellular carcinoma and its clinical implications.Biological procedures online · 2025Review
- Long non-coding RNA in hepatocellular carcinoma: mechanistic insights and therapeutic perspectives.Cellular oncology (Dordrecht, Netherlands) · 2025Review
- Molecular network of metabolic reprogramming and precision diagnosis and treatment of hepatocellular carcinoma.Biomarker research · 2025Review
- CAMKK2 restored mitochondrial dynamics homeostasis to alleviate pulmonary fibrosis via AMPK/PGC-1α signaling pathway in lung fibroblasts.Molecular medicine (Cambridge, Mass.) · 2025Article
- Copper metabolism and cuproptosis: broad perspectives in the treatment of hepatocellular carcinoma.Frontiers in oncology · 2025Review
- MiR-133a-5p Facilitates Cuproptosis in Hepatocellular Carcinoma Through Targeting of ATP7B.Journal of inflammation research · 2025Article
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
backgroundMetabolic reprogramming is a hallmark of hepatocellular carcinoma (HCC) progression, driving aberrant cellular processes in response to pathological stimuli. While dihydrolipoyl transacetylase (DLAT) has been implicated in the development of various cancers, its specific role and underlying mechanisms in HCC remain unclear. This study aimed to investigate the expression, function, and mechanistic impact of DLAT in HCC.
methodsA comprehensive analysis was conducted using RNA sequencing data, tissue microarrays, in vitro and in vivo functional assays, and mechanistic studies to evaluate DLAT expression, its functional role in tumor progression, and associated molecular pathways in HCC.
resultsOur study revealed a significant upregulation of DLAT expression in HCC, which was linked to a poor prognosis. Furthermore, we discovered that DLAT facilitated tumor metastasis by driving metabolic reprogramming in HCC cells. Mechanistically, DLAT was found to enhance glucose transporter 1 (GLUT1) expression via H3K18 acetylation, thereby promoting aerobic glycolysis and epithelial-to-mesenchymal transition (EMT), which subsequently augmented metastasis of HCC both in vitro and in vivo. Finally, we confirmed a positive correlation between DLAT and GLUT1 expression in HCC tissues.
conclusionsThese findings establish DLAT as a key regulator in HCC progression and suggest its potential as a promising predictive biomarker and therapeutic target for improving HCC diagnosis and treatment.
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