ArticlePloS one2010
Point mutations in c-Myc uncouple neoplastic transformation from multiple other phenotypes in rat fibroblasts.
Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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
16 citing papers in PubMed, 23 citations in OpenAlex.
- Combined Inactivation of CTPS1 and ATR Is Synthetically Lethal to MYC-Overexpressing Cancer Cells.Cancer research · 2022Article
- Reticular Dysgenesis and Mitochondriopathy Induced by Adenylate Kinase 2 Deficiency with Atypical Presentation.Scientific reports · 2019Article
- Myc and ChREBP transcription factors cooperatively regulate normal and neoplastic hepatocyte proliferation in mice.The Journal of biological chemistry · 2018Article
- Activated gastric cancer-associated fibroblasts contribute to the malignant phenotype and 5-FU resistance via paracrine action in gastric cancer.Cancer cell international · 2018Article
- MYCbase: a database of functional sites and biochemical properties of Myc in both normal and cancer cells.BMC bioinformatics · 2017Article
- Mitochondrial targeted β-lapachone induces mitochondrial dysfunction and catastrophic vacuolization in cancer cells.Bioorganic & medicinal chemistry letters · 2015Article
- Perturbation of the c-Myc-Max protein-protein interaction via synthetic α-helix mimetics.Journal of medicinal chemistry · 2015Article
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- Alterations in c-Myc phenotypes resulting from dynamin-related protein 1 (Drp1)-mediated mitochondrial fission.Cell death & disease · 2013Article
- Metabolic symbiosis in cancer: refocusing the Warburg lens.Molecular carcinogenesis · 2013Review
- Oxidants and not alkylating agents induce rapid mtDNA loss and mitochondrial dysfunction.DNA repair · 2012Article
- β-catenin is a central mediator of pro-fibrotic Wnt signaling in systemic sclerosis.Annals of the rheumatic diseases · 2012Article
- Article
- The rate of oxygen utilization by cells.Free radical biology & medicine · 2011Article
- c-Myc induction of programmed cell death may contribute to carcinogenesis: a perspective inspired by several concepts of chemical carcinogenesis.Cancer biology & therapy · 2011Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Deregulation of c-Myc (Myc) occurs in many cancers. In addition to transforming various cell types, Myc also influences additional transformation-associated cellular phenotypes including proliferation, survival, genomic instability, reactive oxygen species production, and metabolism. Although Myc is wild type in most cancers (wtMyc), it occasionally acquires point mutations in certain lymphomas. Some of these mutations confer a survival advantage despite partially attenuating proliferation and transformation. Here, we have evaluated four naturally-occurring or synthetic point mutations of Myc for their ability to affect these phenotypes, as well as to promote genomic instability, to generate reactive oxygen species and to up-regulate aerobic glycolysis and oxidative phosphorylation. Our findings indicate that many of these phenotypes are genetically and functionally independent of one another and are not necessary for transformation. Specifically, the higher rate of glucose metabolism known to be associated with wtMyc deregulation was found to be independent of transformation. One mutation (Q131R) was greatly impaired for nearly all of the studied Myc phenotypes, yet was able to retain some ability to transform. These findings indicate that, while the Myc phenotypes examined here make additive contributions to transformation, none, with the possible exception of increased reliance on extracellular glutamine for survival, are necessary for achieving this state.
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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.