ArticleCancer & metabolism2024
Deficiency of TOP1MT enhances glycolysis through the stimulation of PDK4 expression in gastric cancer.
Article in Cancer & metabolism, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 8 citations in OpenAlex.
- Renal single-nucleus transcriptomic of a new model of cardiovascular-kidney-metabolic syndrome in aging swine.American journal of physiology. Renal physiology · 2026Article
- Development and validation of a prognostic prediction model for gastric cancer based on lipophagy-related genes.Translational cancer research · 2025Article
- Oxidative and Glycolytic Metabolism: Their Reciprocal Regulation and Dysregulation in Cancer.Cells · 2025Review
- Multiple data sets to explore the key molecules and mechanism of lymph node metastasis in gastric cancer.Discover oncology · 2025Article
- Targeting Txnip-mediated metabolic reprogramming has therapeutic potential for osteoarthritis.Cell death discovery · 2025Article
- Advances in glycolysis research in gastric cancer: molecular mechanisms, regulatory networks, and therapeutic potential.Frontiers in oncology · 2025Review
- Harnessing glycolysis in gastric cancer: molecular targets, therapeutic strategies, and clinical horizons.Frontiers in immunology · 2025Review
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundAbnormal glucose metabolism is one of the determinants of maintaining malignant characteristics of cancer. Targeting cancer metabolism is regarded as a new strategy for cancer treatment. Our previous studies have found that TOP1MT is a crucial gene that inhibits glycolysis and cell metastasis of gastric cancer (GC) cells, but the mechanism of its regulation of glycolysis remains unclear.
methodsTranscriptome sequencing data, clinic-pathologic features of GC from a variety of public databases, and WGCNA were used to identify novel targets of TOP1MT. Immunohistochemical results of 250 patients with GC were used to analyze the relative expression relationship between TOP1MT and PDK4. The function of TOP1MT was investigated by migration assays and sea-horse analysis in vitro.
resultsWe discovered a mitochondrial topoisomerase I, TOP1MT, which correlated with a higher risk of metastasis. Functional experiments revealed that TOP1MT deficiency promotes cell migration and glycolysis through increasing PDK4 expression. Additionally, the stimulating effect of TOP1MT on glycolysis may be effectively reversed by PDK4 inhibitor M77976.
conclusionsIn brief, our work demonstrated the critical function of TOP1MT in the regulation of glycolysis by PDK4 in gastric cancer. Inhibiting glycolysis and limiting tumor metastasis in GC may be accomplished by suppressing PDK4.
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