ArticleCancer prevention research (Philadelphia, Pa.)2015
UCP2 knockout suppresses mouse skin carcinogenesis.
Article in Cancer prevention research (Philadelphia, Pa.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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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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Who cites it
14 citing papers in PubMed, 27 citations in OpenAlex.
- RNA-DNA Differences: Mechanisms, Oxidative Stress, Transcriptional Fidelity, and Health Implications.Antioxidants (Basel, Switzerland) · 2025Review
- UCP2 and pancreatic cancer: conscious uncoupling for therapeutic effect.Cancer metastasis reviews · 2024Review
- Diabetes Mellitus and Thyroid Cancers: Risky Correlation, Underlying Mechanisms and Clinical Prevention.Diabetes, metabolic syndrome and obesity : targets and therapy · 2024Review
- Genipin, an Inhibitor of UCP2 as a Promising New Anticancer Agent: A Review of the Literature.International journal of molecular sciences · 2022Review
- Glutamine-Derived Aspartate Biosynthesis in Cancer Cells: Role of Mitochondrial Transporters and New Therapeutic Perspectives.Cancers · 2022Review
- UCP2 silencing restrains leukemia cell proliferation through glutamine metabolic remodeling.Frontiers in immunology · 2022Article
- UCP2 as a Potential Biomarker for Adjunctive Metabolic Therapies in Tumor Management.Frontiers in oncology · 2021Review
- Emerging Roles in the Biogenesis of CytochromeFrontiers in cell and developmental biology · 2019Review
- Mitochondrial Uncoupling Proteins: Subtle Regulators of Cellular Redox Signaling.Antioxidants & redox signaling · 2018Review
- The emerging role of immune dysfunction in mitochondrial diseases as a paradigm for understanding immunometabolism.Metabolism: clinical and experimental · 2018Review
- UCP2 overexpression enhanced glycolysis via activation of PFKFB2 during skin cell transformation.Oncotarget · 2017Article
- UCP2 upregulation promotes PLCγ-1 signaling during skin cell transformation.Molecular carcinogenesis · 2017Article
- Uncoupling protein 2 and metabolic diseases.Mitochondrion · 2017Review
- Mitochondrial uncoupling links lipid catabolism to Akt inhibition and resistance to tumorigenesis.Nature communications · 2015Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
Mitochondrial uncoupling (uncouples electron transport from ATP production) has recently been proposed as a novel survival mechanism for cancer cells, and reduction in free radical generation is the accepted mechanism of action. However, there is no direct evidence supporting that uncoupling proteins promote carcinogenesis. Herein, we examined whether mitochondrial uncoupling affects mouse skin carcinogenesis using uncoupling protein 2 (UCP2) homozygous knockout and wild-type mice. The results indicate that knockout of Ucp2 significantly reduced the formation of both benign (papilloma) and malignant (squamous cell carcinoma) tumors. UCP2 knockout did not cause increases in apoptosis during skin carcinogenesis. The rates of oxygen consumption were decreased only in the carcinogen-treated UCP2 knockout mice, whereas glycolysis was increased only in the carcinogen-treated wild-type mice. Finally, the levels of metabolites pyruvate, malate, and succinate showed different trends after carcinogen treatments between the wild-type and UCP2 knockout mice. Our study is the first to demonstrate that Ucp2 knockout suppresses carcinogenesis in vivo. Together with early studies showing that UCP2 is overexpressed in a number of human cancers, UCP2 could be a potential target for cancer prevention and/or therapy. Cancer Prev Res; 8(6); 487-91. ©2015 AACR.
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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.