ArticleOncotarget2016
TP53 mutation hits energy metabolism and increases glycolysis in breast cancer.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 64 citations in OpenAlex.
- Article
- Review
- TP53 deficiency in AML induces resistance to T-cell engagers through an immunosuppressive secretome.Leukemia · 2026Article
- Metabolic Regulation of Immune Responses: Molecular Mechanisms, Diseases, and Therapeutic Targets.MedComm · 2026Review
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- Navigating the Metabolic-Genomic Paradigm: Mitochondrial Reprogramming as a Driver of Cancer Plasticity.Oncology research · 2026Review
- PI5P4Kα promotes glucose and iron acquisition to support metabolic fitness in pancreatic cancer.Cell reports · 2025Article
- Identification of breast cancer subtypes and drug response prediction through forward and reverse translation.NPJ precision oncology · 2025Article
- The Overlapping Biology of Sepsis and Cancer and Therapeutic Implications.Biomedicines · 2025Review
- Comprehensive Bioinformatics Analysis and Validation of the Mechanism of Glutamic-pyruvic Transaminase 2 in Bladder Cancer.Journal of Cancer · 2025Article
- The role of transketolase in the immunotherapy and prognosis of hepatocellular carcinoma: a multi-omics approach.Frontiers in immunology · 2025Article
- Rewired glycolysis by DTL accelerates oncometabolite L-lactate generation to promote breast cancer progression.Frontiers in oncology · 2025Article
- Polycystic Ovary Syndrome and Ferroptosis: Following Ariadne's Thread.Biomedicines · 2024Article
- Glycemic load impacts the response of acquired resistance in breast cancer cells to chemotherapeutic drugs in vitro.PloS one · 2024Article
- Association of Tumor Cell Metabolic Subtype and Immune Response With the Clinical Course of Hepatocellular Carcinoma.The oncologist · 2023Article
- TP53 somatic mutations in Asian breast cancer are associated with subtype-specific effects.Breast cancer research : BCR · 2023Article
- Review
- Differential gene expression of immunity and inflammation genes in colorectal cancer using targeted RNA sequencing.Frontiers in oncology · 2023Article
- The antioxidative stress regulator Nrf2 potentiates radioresistance of oral squamous cell carcinoma accompanied with metabolic modulation.Laboratory investigation; a journal of technical methods and pathology · 2022Article
- Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Promising new hallmarks of cancer is alteration of energy metabolism that involves molecular mechanisms shifting cancer cells to aerobe glycolysis. Our goal was to evaluate the correlation between mutation in the commonly mutated tumor suppressor gene TP53 and metabolism. We established a database comprising mutation and RNA-seq expression data of the TCGA repository and performed receiver operating characteristics (ROC) analysis to compare expression of each gene between TP53 mutated and wild type samples. All together 762 breast cancer samples were evaluated of which 215 had TP53 mutation. Top up-regulated metabolic genes include glycolytic enzymes (e.g. HK3, GPI, GAPDH, PGK1, ENO1), glycolysis regulator (PDK1) and pentose phosphate pathway enzymes (PGD, TKT, RPIA). Gluconeogenesis enzymes (G6PC3, FBP1) were down-regulated. Oxygen consumption and extracellular acidification rates were measured in TP53 wild type and mutant breast cell lines with a microfluorimetric analyzer. Applying metabolic inhibitors in the presence and absence of D-glucose and L-glutamine in cell culture experiments resulted in higher glycolytic and mitochondrial activity in TP53 mutant breast cancer cell lines. In summary, TP53 mutation influences energy metabolism at multiple levels. Our results provide evidence for the synergistic activation of multiple hallmarks linking to these the mutation status of a key driver gene.
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