ArticleBreast cancer research and treatment2015
Combined inhibition of glycolysis and AMPK induces synergistic breast cancer cell killing.
Article in Breast cancer research and treatment, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.
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Who cites it
29 citing papers in PubMed, 1 synthesis or guideline pooled it, 52 citations in OpenAlex.
- A novel miR-1291-ERRα-CPT1C axis modulates tumor cell proliferation, metabolism and tumorigenesis.Theranostics · 2020Pooled it
- Review
- Targeting GSTZ1 Sensitizes KRASG12C-Mutant Lung Cancer Cells by Overcoming Glutathione and Glycolysis Pathway Rewiring.Cancer research communications · 2026Article
- CSN5 overexpression promotes the integral progression of cervical cancer by enhancing ENO3-mediated glycolysis.Apoptosis : an international journal on programmed cell death · 2026Article
- Path-MGCN: a pathway activity-based multi-view graph convolutional network for determining spatial domains.Briefings in bioinformatics · 2025Article
- To be or not to be a fat burner, that is the question for cpt1c in cancer cells.Cell death & disease · 2023Review
- Novel Anti-Cancer Products Targeting AMPK: Natural Herbal Medicine against Breast Cancer.Molecules (Basel, Switzerland) · 2023Review
- Cpt1c Downregulation Causes Plasma Membrane Remodelling and Anthracycline Resistance in Breast Cancer.International journal of molecular sciences · 2023Article
- A Novel Metabolic Reprogramming Strategy for the Treatment of Diabetes-Associated Breast Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Article
- Breast Cancer Cell Subtypes Display Different Metabolic Phenotypes That Correlate with Their Clinical Classification.Biology · 2021Article
- AMPK-Mediated Metabolic Switching Is High Effective for Phytochemical Levo-Tetrahydropalmatine (l-THP) to Reduce Hepatocellular Carcinoma Tumor Growth.Metabolites · 2021Article
- The role of HIF-1α in BCG-stimulated macrophages polarization and their tumoricidal effects in vitro.Medical microbiology and immunology · 2021Article
- The rate of aerobic glycolysis is a pivotal regulator of tumor progression.Journal of diabetes and metabolic disorders · 2021Article
- Continuous flow synthesis of lipophilic cations derived from benzoic acid as new cytotoxic chemical entities in human head and neck carcinoma cell lines.RSC medicinal chemistry · 2020Article
- Coenzyme Q10 in association with metabolism-related AMPK/PFKFB3 and angiogenic VEGF/VEGFR2 genes in breast cancer patients.Molecular biology reports · 2020Article
- PP2Cδ inhibits p300-mediated p53 acetylation via ATM/BRCA1 pathway to impede DNA damage response in breast cancer.Science advances · 2019Article
- Cardamonin inhibits breast cancer growth by repressing HIF-1α-dependent metabolic reprogramming.Journal of experimental & clinical cancer research : CR · 2019Article
- Metabolic Regulation of Glycolysis and AMP Activated Protein Kinase Pathways during Black Raspberry-Mediated Oral Cancer Chemoprevention.Metabolites · 2019Article
- Targeting of PP2Cδ By a Small Molecule C23 Inhibits High Glucose-Induced Breast Cancer ProgressionAntioxidants & redox signaling · 2019Article
- AMP-activated protein kinase: a potential therapeutic target for triple-negative breast cancer.Breast cancer research : BCR · 2019Review
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
Targeting glycolysis for cancer treatment has been investigated as a therapeutic method but has not offered a feasible chemotherapeutic strategy. Our aim was to examine whether AMP-activated protein kinase (AMPK), a conditional oncogene, rescues the energetic stress and cytotoxicity induced by 2-deoxyglucose (2-DG), a glycolytic inhibitor, and the related mechanisms. Luciferin/luciferase adenosine triphosphate (ATP) determination, Western analysis, qRT-PCR analyses, MTT growth assay, clonogenic assay, and statistical analysis were performed in this study. 2-DG decreased ATP levels and subsequently activated AMPK, which contribute to intracellular ATP recovery in MCF-7 cells thus exhibiting no apparent cytotoxicity. Compound C, an AMPK inhibitor, further potentiates 2-DG-induced decrease in ATP levels and inhibits their recovery. 2-DG, via AMPK activation, stimulated cAMP response element-binding protein (CREB) phosphorylation and activity and promoted nuclear peroxisome proliferator-activated receptor gamma coactivator-1-beta (PGC-1β) and estrogen-related receptor α (ERRα) protein expression, leading to augmented mitochondrial biogenesis and expression of fatty acid oxidation (FAO) genes including PPARα, MCAD, CPT1C, and ACO. This metabolic adaptation elicited by AMPK counteracts the ATP-depleting and cancer cell-killing effect of 2-DG. However, 2-DG in combination with AMPK antagonists or small interfering RNA caused a dramatic increase in cytotoxicity in MCF-7 but not in MCF-10A cells. Similarly, when combined with inhibition of CREB/PGC-1β/ERRα pathway, 2-DG saliently suppressed mitochondrial biogenesis and the expression of FAO genes, depleted ATP production, and enhanced cytotoxicity in cancer cells. Collectively, the combination of 2-DG and AMPK inhibition synergistically enhanced the cytotoxic potential in breast cancer cells with a relative nontoxicity to normal cells and may offer a promising, safe, and effective breast cancer therapeutic strategy.
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