ArticleOncotarget2016
Synonymous mutations in oncogenesis and apoptosis versus survival unveiled by network modeling.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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
8 citing papers in PubMed, 11 citations in OpenAlex.
- Microbiota as the unifying factor behind the hallmarks of cancer.Journal of cancer research and clinical oncology · 2023Review
- Network modeling-based identification of the switching targets between pyroptosis and secondary pyroptosis.Chaos, solitons, and fractals · 2022Article
- Tumor necrosis factor-α mediated inflammation versus apoptosis in age-related hearing loss.Frontiers in aging neuroscience · 2022Article
- Quantifying the optimal strategy of population control of quorum sensing network in Escherichia coli.NPJ systems biology and applications · 2021Article
- System-based approaches as prognostic tools for glioblastoma.BMC cancer · 2019Review
- Recognition of the polycistronic nature of human genes is critical to understanding the genotype-phenotype relationship.Genome research · 2018Review
- Analysis of Newly Identified and Rare Synonymous Genetic Variants in the RET Gene in Patients with Medullary Thyroid Carcinoma in Polish Population.Endocrine pathology · 2017Article
- Association ofJournal of ophthalmic & vision researchArticle
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Synonymous mutations, which do not alter the encoded amino acid, have been routinely assumed to be 'neutral' and would have no effect on phenotype or fitness. Yet increasing observations have emerged to overturn this conventional concept. However, convicted elucidation of how synonymous mutations exert biological consequences in oncogenesis is still lacking. By performing systematic analysis of the TNF-α signaling network model, we identify the critical dose which separates the cell survival and apoptosis regions and define the sensitive parameters with single-parameter sensitivity analysis. Combining with the cancer-related mutation spectra obtained from 9 cancers, our results hint that, similar as missense and nonsense mutations, synonymous mutations are also strongly correlated with the parameter sensitivity of the critical dose, providing possible causal mechanism of the mutations in cancer development. Based on such a correlation, we furthermore dissect that members of caspases family proteases (caspase3, 6, 8) could jointly inhibit NFκB activation, providing efficient pro-apoptotic behavior. Thus, we argue that apoptosis module could suppress survival module through negative feedback of caspases family on NFκB.
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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.