ArticleOncotarget2014
Metabolic effect of TAp63α: enhanced glycolysis and pentose phosphate pathway, resulting in increased antioxidant defense.
Article in Oncotarget, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 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
43 citing papers in PubMed, 53 citations in OpenAlex.
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- p63 affects distinct metabolic pathways during keratinocyte senescence, evaluated by metabolomic profile and gene expression analysis.Cell death & disease · 2024Article
- Natural Products and Altered Metabolism in Cancer: Therapeutic Targets and Mechanisms of Action.International journal of molecular sciences · 2024Review
- Variation in pentose phosphate pathway-associated metabolism dictates cytotoxicity outcomes determined by tetrazolium reduction assays.Scientific reports · 2023Article
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- Targeting Energy Metabolism in Cancer Treatment.International journal of molecular sciences · 2022Review
- Structural diversity of p63 and p73 isoforms.Cell death and differentiation · 2022Review
- A Risk-Scoring Model Based on Evaluation of Ferroptosis-Related Genes in Osteosarcoma.Journal of oncology · 2022Article
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- Expression ofJournal of ophthalmology · 2021Article
- Multi-omics profiling of calcium-induced human keratinocytes differentiation reveals modulation of unfolded protein response signaling pathways.Cell cycle (Georgetown, Tex.) · 2019Article
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- Consensus report of the 8 and 9th Weinman Symposia on Gene x Environment Interaction in carcinogenesis: novel opportunities for precision medicine.Cell death and differentiation · 2018Review
- KLF5 controls glutathione metabolism to suppress p190-BCR-ABL+ B-cell lymphoblastic leukemia.Oncotarget · 2018Article
- When nature's robots go rogue: exploring protein homeostasis dysfunction and the implications for understanding human aging disease pathologies.Expert review of proteomics · 2018Review
- Emerging Roles of p53 Family Members in Glucose Metabolism.International journal of molecular sciences · 2018Review
- Glutaminase inhibition improves FLT3 inhibitor therapy for acute myeloid leukemia.Experimental hematology · 2018Article
- Non-oncogenic roles of TAp73: from multiciliogenesis to metabolism.Cell death and differentiation · 2018Review
- Dysregulated metabolic enzymes and metabolic reprogramming in cancer cells.Biomedical reports · 2018Article
Corrections and comments
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Authors and funding
7 authors at 5 institutions in 4 countries.
Funding
Abstract
TAp63α is a member of the p53 family, which plays a central role in epithelial cancers. Recently, a role has emerged for p53 family members in cancer metabolic modulation. In order to assess whether TAp63α plays a role in cancer metabolism, we exploited p53-null osteosarcoma Tet-On Saos-2 cells, in which the expression of TAp63α was dependent on doxycycline supplementation to the medium. Metabolomics labeling experiments were performed by incubating the cells in 13C-glucose or 13C15N-glutamine-labeled culture media, as to monitor metabolic fluxes upon induced expression of TAp63α. Induced expression of TAp63α resulted in cell cycle arrest at the G1 phase. From a metabolic standpoint, expression of Tap63α promoted glycolysis and the pentose phosphate pathway, which was uncoupled from nucleotide biosynthesis, albeit prevented oxidative stress in the form of oxidized glutathione. Double 13C-glucose and 13C15N-glutamine metabolic labeling confirmed that induced expression of TAp63α corresponded to a decreased flux of pyruvate to the Krebs cycle and decreased utilization of glutamine for catabolic purposes in the TCA cycle. Results were not conclusive in relation to anabolic utilization of labeled glutamine, since it is unclear to what extent the observed minor TAp63α-dependent increases of glutamine-derived labeling in palmitate could be tied to increased rates of reductive carboxylation and de novo synthesis of fatty acids. Finally, bioinformatics elaborations highlighted a link between patient survival rates and the co-expression of p63 and rate limiting enzymes of the pentose phosphate pathway, G6PD and PGD.
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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.