ArticleCell death discovery2019
Low-dose 2-deoxyglucose and metformin synergically inhibit proliferation of human polycystic kidney cells by modulating glucose metabolism.
Article in Cell death discovery, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
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Who cites it
23 citing papers in PubMed, 50 citations in OpenAlex.
- The moonlighting functions of glycolytic enzymes in tumorigenesis.Cellular oncology (Dordrecht, Netherlands) · 2026Review
- 2-Deoxy-D-Glucose restores glial cell mitochondrial function and attenuates neuroinflammation.Scientific reports · 2025Article
- Harnessing metabolic control for synaptic stability: REST/NRSF links glycolytic inhibition to excitatory neurotransmission.The Journal of physiology · 2025Article
- Metformin as a Disease-Modifying Agent in Autosomal Dominant Polycystic Kidney Disease: A Systematic Review of Preclinical and Clinical Evidence.Current issues in molecular biology · 2025Review
- Antiproliferative effects of dihydrotanshinone I on autosomal dominant polycystic kidney disease via immunomodulation.The Journal of pharmacology and experimental therapeutics · 2025Article
- Methods and Guidelines for Metabolism Studies: Applications to Cancer Research.International journal of molecular sciences · 2025Review
- Metabolism, a Blossoming Target for Small-Molecule Anticancer Drugs.Molecules (Basel, Switzerland) · 2025Review
- Metabolic Reprogramming in Autosomal Dominant Polycystic Kidney Disease: Role in Cystogenesis and Novel Therapeutic Approaches.Biomedicines · 2025Review
- Glucose transporter 2‑transported glucosamine inhibits glycolysis in cancer cell lines through competition with glucose for hexokinase II.Oncology reports · 2025Article
- Metformin Use and Clinical Outcomes in Autosomal Dominant Polycystic Kidney Disease: A Nationwide Cohort Study.Biomedicines · 2025Article
- Physiologically Achievable Concentration of 2-Deoxy-D-Glucose Stimulates IFN-γ Secretion in Activated T Cells In Vitro.International journal of molecular sciences · 2024Article
- Mycobacterium tuberculosis produces D-serine under hypoxia to limit CD8Nature microbiology · 2024Article
- Article
- DNA Aptamer Beacon Probe (ABP) for Monitoring of Adenosine Triphosphate Level in SW480 Cancer Cells Treated with Glycolysis Inhibitor 2-Deoxyglucose.International journal of molecular sciences · 2023Article
- Genetic mutations affecting mitochondrial function in cancer drug resistance.Genes & genomics · 2023Review
- Non-metabolic functions of phosphofructokinase-1 orchestrate tumor cellular invasion and genome maintenance under bevacizumab therapy.Neuro-oncology · 2023Article
- Combining Metformin and Drug-Loaded Kidney-Targeting Micelles for Polycystic Kidney Disease.Cellular and molecular bioengineering · 2023Article
- 2-Deoxy-D-Glucose: A Novel Pharmacological Agent for Killing Hypoxic Tumor Cells, Oxygen Dependence-Lowering in Covid-19, and Other Pharmacological Activities.Advances in pharmacological and pharmaceutical sciences · 2023Review
- Role of abnormal energy metabolism in the progression of chronic kidney disease and drug intervention.Renal failure · 2022Article
- Strategies for the induction of anti-inflammatory mesenchymal stem cells and their application in the treatment of immune-related nephropathy.Frontiers in medicine · 2022Review
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Polycystic kidney disease (PKD) is a common hereditary kidney disease with abnormal proliferation and apoptosis of kidney cystic epithelial cells, eventually leading to chronic renal failure. Currently, there are no effective treatment methods. Similar to tumor cells, cystic epithelial cells have abnormal glycolysis and over-activation of proliferation signaling pathways. In the present study, for the first time, we investigated the effects of low-dose combinational use of 2-deoxyglucose (2-DG) and metformin (MET) on the proliferation and apoptosis in the human cystic kidney epithelial cells. Cystic epithelia cells were divided into control group, 2-DG group, MET group and 2-DG+MET group. Cell Proliferation, apoptosis and glucose metabolism were measured in each group. The results showed that low-dose combinational treatment of 2-DG and MET significantly inhibited the proliferation of renal cystic epithelial cells by suppressing the activities of PKA, mTOR and ERK signaling pathways and upregulating PI3K/Akt pathway. Combination of both drugs increased the apoptosis rates of cystic epithelial cells. Two drugs inhibited glucose metabolic phenotypes, glycolysis and oxidative phosphorylation, and significantly lowered the intracellular ATP level in cystic epithelial cells. 2-DG could also neutralize excessive production of lactate (lactic acidosis) caused by MET and both drugs had complementary effect for cystic epithelial cells. These results reveal that combinational use of low-dose 2-DG and MET can markedly inhibit proliferation via modulating glucose metabolic phenotypes in human polycystic kidney epithelial cells, low-dose combinational use of both drugs can also lower the toxic effects of each drug, and is a novel strategy for future treatment of human polycystic kidney disease.
Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.