ArticlePloS one2017
Overexpression of the human DEK oncogene reprograms cellular metabolism and promotes glycolysis.
Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
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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
20 citing papers in PubMed, 30 citations in OpenAlex.
- All hands on DEK: structural insights into a unique histone modifier and chromatin remodeler.Epigenetics & chromatin · 2026Review
- Dek Loss Induces Sex-Dependent, Task-Specific Cognitive Deficits and Reprograms the Hippocampal Transcriptome in Mice.Research square · 2025Article
- DEK promotes mammary hyperplasia and is associated with H3K27me3 epigenetic modifications.Life science alliance · 2025Article
- NMR-Based Stable Isotope Tracing of Cancer Metabolism.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Review
- Lactate Activates AMPK Remodeling of the Cellular Metabolic Profile and Promotes the Proliferation and Differentiation of C2C12 Myoblasts.International journal of molecular sciences · 2022Article
- En masse organoid phenotyping informs metabolic-associated genetic susceptibility to NASH.Cell · 2022Article
- In silico gene expression and pathway analysis of DEK in the human brain across the lifespan.The European journal of neuroscience · 2022Article
- Novel molecular mechanisms in Alzheimer's disease: The potential role of DEK in disease pathogenesis.Frontiers in aging neuroscience · 2022Review
- Article
- Role of GM-CSF in regulating metabolism and mitochondrial functions critical to macrophage proliferation.Mitochondrion · 2022Article
- MAPK1/3 kinase-dependent ULK1 degradation attenuates mitophagy and promotes breast cancer bone metastasis.Autophagy · 2021Article
- PKM2-dependent metabolic skewing of hepatic Th17 cells regulates pathogenesis of non-alcoholic fatty liver disease.Cell metabolism · 2021Article
- DEK is highly expressed in breast cancer and is associated with malignant phenotype and progression.Oncology letters · 2021Article
- DEK Expression in Breast Cancer Cells Leads to the Alternative Activation of Tumor Associated Macrophages.Cancers · 2020Article
- Optical Redox Imaging Detects the Effects of DEK Oncogene Knockdown on the Redox State of MDA-MB-231 Breast Cancer Cells.Molecular imaging and biology · 2019Article
- NMR-based metabolomic analysis of the effects of alanyl-glutamine supplementation on C2C12 myoblasts injured by energy deprivation.RSC advances · 2018Article
- Dek overexpression in murine epithelia increases overt esophageal squamous cell carcinoma incidence.PLoS genetics · 2018Article
- The nuclear DEK interactome supports multi-functionality.Proteins · 2018Article
- Cancer Cell Metabolism: Implications for X-ray and Particle Radiation Therapy.International journal of particle therapy · 2018Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
The DEK oncogene is overexpressed in many human malignancies including at early tumor stages. Our reported in vitro and in vivo models of squamous cell carcinoma have demonstrated that DEK contributes functionally to cellular and tumor survival and to proliferation. However, the underlying molecular mechanisms remain poorly understood. Based on recent RNA sequencing experiments, DEK expression was necessary for the transcription of several metabolic enzymes involved in anabolic pathways. This identified a possible mechanism whereby DEK may drive cellular metabolism to enable cell proliferation. Functional metabolic Seahorse analysis demonstrated increased baseline and maximum extracellular acidification rates, a readout of glycolysis, in DEK-overexpressing keratinocytes and squamous cell carcinoma cells. DEK overexpression also increased the maximum rate of oxygen consumption and therefore increased the potential for oxidative phosphorylation (OxPhos). To detect small metabolites that participate in glycolysis and the tricarboxylic acid cycle (TCA) that supplies substrate for OxPhos, we carried out NMR-based metabolomics studies. We found that high levels of DEK significantly reprogrammed cellular metabolism and altered the abundances of amino acids, TCA cycle intermediates and the glycolytic end products lactate, alanine and NAD+. Taken together, these data support a scenario whereby overexpression of the human DEK oncogene reprograms keratinocyte metabolism to fulfill energy and macromolecule demands required to enable and sustain cancer cell growth.
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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.