ArticleCancer science2018
Aldo-keto reductases-mediated cytotoxicity of 2-deoxyglucose: A novel anticancer mechanism.
Article in Cancer science, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
10 citing papers in PubMed, 1 synthesis or guideline pooled it, 18 citations in OpenAlex.
- Advances and prospects in deuterium metabolic imaging (DMI): a systematic review of in vivo studies.European radiology experimental · 2024Pooled it
- Tempol, a Superoxide Dismutase Mimetic, Inhibits Wallerian Degeneration Following Spinal Cord Injury by Preventing Glutathione Depletion and Aldose Reductase Activation.Journal of neurotrauma · 2024Article
- Exploration and validation of a novel reactive oxygen species-related signature for predicting the prognosis and chemotherapy response of patients with bladder cancer.Frontiers in immunology · 2024Article
- Unveiling the veil of lactate in tumor-associated macrophages: a successful strategy for immunometabolic therapy.Frontiers in immunology · 2023Review
- In Silico Evaluation of Binding of 2-Deoxy-D-Glucose with Mpro of nCoV to Combat COVID-19.Pharmaceutics · 2022Article
- Role of aldo-keto reductase family 1 member B1 (AKR1B1) in the cancer process and its therapeutic potential.Journal of cellular and molecular medicine · 2020Review
- The AKR1B1 inhibitor epalrestat suppresses the progression of cervical cancer.Molecular biology reports · 2020Article
- Reactive oxygen species in cancer: a paradox between pro- and anti-tumour activities.Cancer chemotherapy and pharmacology · 2020Review
- Neuroprotection Effect of Astragaloside IV from 2-DG-Induced Endoplasmic Reticulum Stress.Oxidative medicine and cellular longevity · 2020Article
- Aldo-keto reductases-mediated cytotoxicity of 2-deoxyglucose: A novel anticancer mechanism.Cancer science · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
2-Deoxyglucose (2DG) is a non-metabolizable glucose analog currently in clinical trials to determine its efficacy in enhancing the therapeutic effects of radiotherapy and chemotherapy of several types of cancers. It is thought to preferentially kill cancer cells by inhibiting glycolysis because cancer cells are more dependent on glycolysis for their energy needs than normal cells. However, we found that the toxicity of 2DG in cancer cells is mediated by the enzymatic activities of AKR1B1 and/or AKR1B10 (AKR1Bs), which are often overexpressed in cancer cells. Our results show that 2DG kills cancer cells because, in the process of being reduced by AKR1Bs, depletion of their cofactor NADPH leads to the depletion of glutathione (GSH) and cell death. Furthermore, we showed that compounds that are better substrates for AKR1Bs than 2DG are more effective than 2DG in killing cancer cells that overexpressed these 2 enzymes. As cancer cells can be induced to overexpress AKR1Bs, the anticancer mechanism we identified can be applied to treat a large variety of cancers. This should greatly facilitate the development of novel anticancer drugs.
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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 OpenQuestion graph.