ArticleCell cycle (Georgetown, Tex.)2018
Metabolic reprogramming enables hepatocarcinoma cells to efficiently adapt and survive to a nutrient-restricted microenvironment.
Article in Cell cycle (Georgetown, Tex.), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers, 1 of them a synthesis that pooled it.
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Who cites it
73 citing papers in PubMed, 1 synthesis or guideline pooled it.
- The metabolic addiction of cancer stem cells.Frontiers in oncology · 2022Pooled it
- TALDO1 promotes lipid metabolic reprogramming and immunosuppressive microenvironment remodelling in hepatocellular carcinoma.Clinical and translational medicine · 2026Article
- Metabolic reprogramming in cancer: dysregulation of glucose, lipid, and amino acid pathways and therapeutic opportunities.Molecular biomedicine · 2026Review
- FSTL1 Orchestrates Metabolic-Epigenetic Crosstalk: Glycolysis-Dependent H3K18 Lactylation Drives Cartilage Fibrosis in Osteoarthritis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Energy metabolism in health and diseases.Signal transduction and targeted therapy · 2025Review
- Mitochondrial dysfunction-driven AMPK-p53 axis activation underpins the anti-hepatocellular carcinoma effects of sulfane sulfur.Scientific reports · 2025Article
- The impact of metabolic reprogramming in hepatocellular carcinoma on T cell.Frontiers in immunology · 2025Review
- Redox homeostasis of one-carbon metabolism-dependent reprogramming is critical for RCC progression under exogenous serine/glycine-deprived conditions.BMC cancer · 2024Article
- Therapeutic potential of tLyp-1-EV-shCTCF in inhibiting liver cancer stem cell self-renewal and immune escape via SALL3 modulation in hepatocellular carcinoma.Translational oncology · 2024Article
- Decoding sunitinib resistance in ccRCC: Metabolic-reprogramming-induced ABAT and GABAergic system shifts.iScience · 2024Article
- Large enrichments in fatty acidProceedings of the National Academy of Sciences of the United States of America · 2024Article
- Targeting metabolic reprogramming promotes the efficacy of transarterial chemoembolization in the rabbit VX2 liver tumor model.Oncology letters · 2024Article
- The role of metabolic reprogramming in kidney cancer.Frontiers in oncology · 2024Review
- Metabolomics-Guided Identification of a Distinctive Hepatocellular Carcinoma Signature.Cancers · 2023Article
- Pathogenesis of Hepatocellular Carcinoma: The Interplay of Apoptosis and Autophagy.Biomedicines · 2023Review
- The Ketogenic Diet in Colorectal Cancer: A Means to an End.International journal of molecular sciences · 2023Review
- AIM2 upregulation promotes metastatic progression and PD-L1 expression in lung adenocarcinoma.Cancer science · 2023Article
- Unveiling the veil of lactate in tumor-associated macrophages: a successful strategy for immunometabolic therapy.Frontiers in immunology · 2023Review
- Metabolic reprogramming of clear cell renal cell carcinoma.Frontiers in endocrinology · 2023Review
- Phosphoenolpyruvate carboxykinases as emerging targets in cancer therapy.Frontiers in cell and developmental biology · 2023Review
13 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatocellular carcinoma (HCC) is a metabolically heterogeneous cancer and the use of glucose by HCC cells could impact their tumorigenicity. Dt81Hepa1-6 cells display enhanced tumorigenicity compared to parental Hepa1-6 cells. This increased tumorigenicity could be explained by a metabolic adaptation to more restrictive microenvironments. When cultured at high glucose concentrations, Dt81Hepa1-6 displayed an increased ability to uptake glucose (P<0.001), increased expression of 9 glycolytic genes, greater GTP and ATP (P<0.001), increased expression of 7 fatty acid synthesis-related genes (P<0.01) and higher levels of Acetyl-CoA, Citrate and Malonyl-CoA (P<0.05). Under glucose-restricted conditions, Dt81Hepa1-6 used their stored fatty acids with increased expression of fatty acid oxidation-related genes (P<0.01), decreased triglyceride content (P<0.05) and higher levels of GTP and ATP (P<0.01) leading to improved proliferation (P<0.05). Inhibition of lactate dehydrogenase and aerobic glycolysis with sodium oxamate led to decreased expression of glycolytic genes, reduced lactate, GTP and ATP levels (P<0.01), increased cell doubling time (P<0.001) and reduced fatty acid synthesis. When combined with cisplatin, this inhibition led to lower cell viability and proliferation (P<0.05). This metabolic-induced tumorigenicity was also reflected in human Huh7 cells by a higher glucose uptake and proliferative capacity compared to HepG2 cells (P<0.05). In HCC patients, increased tumoral expression of Glut-1, Hexokinase II and Lactate dehydrogenase correlated with poor survival (P = 2.47E
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