ArticleOncogene2010
Glycolysis inhibition sensitizes tumor cells to death receptors-induced apoptosis by AMP kinase activation leading to Mcl-1 block in translation.
Article in Oncogene, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers.
What it found
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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
86 citing papers in PubMed, 137 citations in OpenAlex.
- Metformin in Combination with Standard Therapy in Patients with Diffuse Large B-Cell Lymphoma: A Randomized Phase II Clinical Trial.Asian Pacific journal of cancer prevention : APJCP · 2024Trial
- Cell death and cancer: Metabolic interconnections.Cell reports · 2025Review
- Interactions among nutrition, metabolism and the immune system in the context of starvation and nutrition-stimulated obesity.Nutrition & diabetes · 2025Review
- AMPK-mTOR pathway modulates glycolysis reprogramming in unexplained recurrent spontaneous abortion.BMC pregnancy and childbirth · 2024Article
- Article
- Review
- Glucose oxidation-dependent survival of activated B cells provides a putative novel therapeutic target for lupus treatment.iScience · 2023Article
- BCL-2 protein family: attractive targets for cancer therapy.Apoptosis : an international journal on programmed cell death · 2023Review
- Autophagy and Apoptosis: Current Challenges of Treatment and Drug Resistance in Multiple Myeloma.International journal of molecular sciences · 2022Review
- mTORC1 beyond anabolic metabolism: Regulation of cell death.The Journal of cell biology · 2022Review
- Understanding MCL1: from cellular function and regulation to pharmacological inhibition.The FEBS journal · 2022Review
- Resistance of Human Liver Mesenchymal Stem Cells to FAS-Induced Cell Death.Current issues in molecular biology · 2022Article
- Targeting Glycolysis in Alloreactive T Cells to Prevent Acute Graft-Frontiers in immunology · 2022Article
- Review
- Elevated CLOCK and BMAL1 Contribute to the Impairment of Aerobic Glycolysis from Astrocytes in Alzheimer's Disease.International journal of molecular sciences · 2020Article
- Review
- Saga of Mcl-1: regulation from transcription to degradation.Cell death and differentiation · 2020Review
- By reducing global mRNA translation in several ways, 2-deoxyglucose lowers MCL-1 protein and sensitizes hemopoietic tumor cells to BH3 mimetic ABT737.Cell death and differentiation · 2019Article
- Mechanisms by Which Obesity Impacts Survival from Acute Lymphoblastic Leukemia.Journal of the National Cancer Institute. Monographs · 2019Review
- Review
26 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 7 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Most cancer cells exhibit increased glycolysis for generation of their energy supply. This specificity could be used to preferentially kill these cells. In this study, we identified the signaling pathway initiated by glycolysis inhibition that results in sensitization to death receptor (DR)-induced apoptosis. We showed, in several human cancer cell lines (such as Jurkat, HeLa, U937), that glucose removal or the use of nonmetabolizable form of glucose (2-deoxyglucose) dramatically enhances apoptosis induced by Fas or by tumor necrosis factor-related apoptosis-inducing ligand. This sensitization is controlled through the adenosine monophosphate (AMP)-activated protein kinase (AMPK), which is the central energy-sensing system of the cell. We established the fact that AMPK is activated upon glycolysis block resulting in mammalian target of rapamycin (mTOR) inhibition leading to Mcl-1 decrease, but no other Bcl-2 anti-apoptotic members. Interestingly, we determined that, upon glycolysis inhibition, the AMPK-mTOR pathway controlled Mcl-1 levels neither through transcriptional nor through posttranslational mechanism but rather by controlling its translation. Therefore, our results show a novel mechanism for the sensitization to DR-induced apoptosis linking glucose metabolism to Mcl-1 downexpression. In addition, this study provides a rationale for the combined use of DR ligands with AMPK activators or mTOR inhibitors in the treatment of human cancers.
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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.