ArticleCell death & disease2014
Glucose metabolism and hexosamine pathway regulate oncogene-induced senescence.
Article in Cell death & disease, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 25 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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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
25 citing papers in PubMed, 53 citations in OpenAlex.
- Disruption of metabolic licensing by JAK inhibitors constrains CD8 T cell activation and effector function.Cell death & disease · 2026Article
- Mitochondrial regulation of cellular senescence heterogeneity.Frontiers in cell and developmental biology · 2026Review
- Disruption of metabolic licensing by JAK inhibitors constrains CD8 T cell activation and effector function.Research square · 2025Article
- Cellular Senescence: A Bridge Between Diabetes and Microangiopathy.Biomolecules · 2024Review
- O-GlcNAcylation inhibition redirects the response of colon cancer cells to chemotherapy from senescence to apoptosis.Cell death & disease · 2024Article
- Article
- Branched-Chain Amino Acid Accumulation Fuels the Senescence-Associated Secretory Phenotype.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Senescent Endothelial Cells Sustain Their Senescence-Associated Secretory Phenotype (SASP) through Enhanced Fatty Acid Oxidation.Antioxidants (Basel, Switzerland) · 2023Article
- Review
- SNORA14A inhibits hepatoblastoma cell proliferation by regulating SDHB-mediated succinate metabolism.Cell death discovery · 2023Article
- Revisited Metabolic Control and Reprogramming Cancers by Means of the Warburg Effect in Tumor Cells.International journal of molecular sciences · 2022Review
- Expression of the Calcium-Binding Protein CALB1 Is Induced and Controls Intracellular CaInternational journal of molecular sciences · 2022Article
- RNA sequencing profiles reveal dynamic signaling and glucose metabolic features during bone marrow mesenchymal stem cell senescence.Cell & bioscience · 2022Article
- Hyperoxia causes senescence and increases glycolysis in cultured lung epithelial cells.Physiological reports · 2021Article
- HBXIP Regulates Gastric Cancer Glucose Metabolism and Malignancy Through PI3K/AKT and p53 Signaling.OncoTargets and therapy · 2020Article
- Deconvoluting the dual hypoglycemic effect of wedelolactone isolated fromRSC advances · 2018Article
- Epithelial cell senescence: an adaptive response to pre-carcinogenic stresses?Cellular and molecular life sciences : CMLS · 2017Review
- The cytosolic 5'-nucleotidase cN-II lowers the adaptability to glucose deprivation in human breast cancer cells.Oncotarget · 2017Article
- Analysis of Gene Expression in Human Dermal Fibroblasts Treated with Senescence-Modulating COX Inhibitors.Genomics & informatics · 2017Article
- Multidrug resistance protein 3 loss promotes tumor formation by inducing senescence escape.Oncogene · 2016Article
Corrections and comments
- Erratum issued
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Oncogenic stress-induced senescence (OIS) prevents the ability of oncogenic signals to induce tumorigenesis. It is now largely admitted that the mitogenic effect of oncogenes requires metabolic adaptations to respond to new energetic and bio constituent needs. Yet, whether glucose metabolism affects OIS response is largely unknown. This is largely because of the fact that most of the OIS cellular models are cultivated in glucose excess. In this study, we used human epithelial cells, cultivated without glucose excess, to study alteration and functional role of glucose metabolism during OIS. We report a slowdown of glucose uptake and metabolism during OIS. Increasing glucose metabolism by expressing hexokinase2 (HK2), which converts glucose to glucose-6-phosphate (G6P), favors escape from OIS. Inversely, expressing a glucose-6-phosphatase, [corrected] pharmacological inhibition of HK2, or adding nonmetabolizable glucose induced a premature senescence. Manipulations of various metabolites covering G6P downstream pathways (hexosamine, glycolysis, and pentose phosphate pathways) suggest an unexpected role of the hexosamine pathway in controlling OIS. Altogether, our results show that decreased glucose metabolism occurs during and participates to OIS.
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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.