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• W2009987946 endingPage "e1003455" @default.
• W2009987946 startingPage "e1003455" @default.
• W2009987946 abstract "Recently, a molecular pathway linking inflammation to cell transformation has been discovered. This molecular pathway rests on a positive inflammatory feedback loop between NF-κB, Lin28, Let-7 microRNA and IL6, which leads to an epigenetic switch allowing cell transformation. A transient activation of an inflammatory signal, mediated by the oncoprotein Src, activates NF-κB, which elicits the expression of Lin28. Lin28 decreases the expression of Let-7 microRNA, which results in higher level of IL6 than achieved directly by NF-κB. In turn, IL6 can promote NF-κB activation. Finally, IL6 also elicits the synthesis of STAT3, which is a crucial activator for cell transformation. Here, we propose a computational model to account for the dynamical behavior of this positive inflammatory feedback loop. By means of a deterministic model, we show that an irreversible bistable switch between a transformed and a non-transformed state of the cell is at the core of the dynamical behavior of the positive feedback loop linking inflammation to cell transformation. The model indicates that inhibitors (tumor suppressors) or activators (oncogenes) of this positive feedback loop regulate the occurrence of the epigenetic switch by modulating the threshold of inflammatory signal (Src) needed to promote cell transformation. Both stochastic simulations and deterministic simulations of a heterogeneous cell population suggest that random fluctuations (due to molecular noise or cell-to-cell variability) are able to trigger cell transformation. Moreover, the model predicts that oncogenes/tumor suppressors respectively decrease/increase the robustness of the non-transformed state of the cell towards random fluctuations. Finally, the model accounts for the potential effect of competing endogenous RNAs, ceRNAs, on the dynamics of the epigenetic switch. Depending on their microRNA targets, the model predicts that ceRNAs could act as oncogenes or tumor suppressors by regulating the occurrence of cell transformation." @default.
• W2009987946 created "2016-06-24" @default.
• W2009987946 creator A5020843492 @default.
• W2009987946 creator A5059875969 @default.
• W2009987946 creator A5083348243 @default.
• W2009987946 creator A5088550648 @default.
• W2009987946 date "2014-01-30" @default.
• W2009987946 modified "2023-09-24" @default.
• W2009987946 title "A Model for the Epigenetic Switch Linking Inflammation to Cell Transformation: Deterministic and Stochastic Approaches" @default.
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• W2009987946 doi "https://doi.org/10.1371/journal.pcbi.1003455" @default.
• W2009987946 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3907303" @default.
• W2009987946 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/24499937" @default.
• W2009987946 hasPublicationYear "2014" @default.
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