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Epithelial to mesenchymal transition (EMT) is a complex biological process that plays a key role in cancer progression and metastasis formation. Its activation results in epithelial cells losing adhesion and polarity and becoming capable of migrating from their site of origin. At this step the disease is generally considered incurable. As EMT execution involves several individual molecular components, connected by nontrivial relations, in vitro techniques are often inadequate to capture its complexity. Computational models can be used to complement experiments and provide additional knowledge difficult to build up in a wetlab. Indeed in silico analysis gives the user total control on the system, allowing to identify the contribution of each independent element. In the following, two kinds of approaches to the computational study of EMT will be presented. The first relies on signal transduction networks description and details how changes in gene expression could influence this process, both focusing on specific aspects of the EMT and providing a general frame for this phenomenon easily comparable with experimental data. The second integrates single cell and population level descriptions in a multiscale model that can be considered a more accurate representation of the EMT. The advantages and disadvantages of each approach will be highlighted, together with the importance of coupling computational and experimental results. Finally, the main challenges that need to be addressed to improve our knowledge of the role of EMT in the neoplastic disease and the scientific and translational value of computational models in this respect will be presented. This article is categorized under: Analytical and Computational Methods > Computational Methods.
This article was published in the following journal.
Name: Wiley interdisciplinary reviews. Systems biology and medicine
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Phenotypic changes of EPITHELIAL CELLS to MESENCHYME type, which increase cell mobility critical in many developmental processes such as NEURAL TUBE development. NEOPLASM METASTASIS and DISEASE PROGRESSION may also induce this transition.
Models connecting initiating events at the cellular and molecular level to population-wide impacts. Computational models may be at levels relating toxicology to adverse effects.
A highly-conserved family of basic helix-loop-helix (bHLH) transcription factors. They function as dimers with other bHLH proteins and bind E-BOX ELEMENTS to control gene expression during EMBRYOGENESIS and the EPITHELIAL-MESENCHYMAL TRANSITION.
A transcription factor family characterized by the presence of several C-terminal CYS2-HIS2 ZINC FINGERS. They function in many developmental processes including the induction of the EPITHELIAL-MESENCHYMAL TRANSITION; maintenance of embryonic MESODERM; growth arrest, CELL SURVIVAL; and CELL MIGRATION.
A transcription factor characterized by N-terminal and C-terminal CYS2-HIS2 ZINC FINGERS separated by a homeobox. It represses the expression of E-CADHERIN to induce the EPITHELIAL-MESENCHYMAL TRANSITION. It also represses PROTO-ONCOGENE PROTEINS C-BCL-6; regulates the cell type-specific expression of SODIUM-POTASSIUM-EXCHANGING ATPASE; and promotes neuronal differentiation.
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