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Transcriptomic and computational analysis identified LPA metabolism, KLHL14 and KCNE3 as novel regulators of Epithelial-Mesenchymal Transition
Epithelial-mesenchymal transition (EMT) is a complex biological program between physiology and pathology. Here, amniotic epithelial cells (AEC) were used as in vitro model of transiently inducible EMT in order to evaluate the transcriptional insights underlying this process. Therefore, RNA-seq was u...
Autores principales: | , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7060278/ https://www.ncbi.nlm.nih.gov/pubmed/32144311 http://dx.doi.org/10.1038/s41598-020-61017-y |
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author | Di Lollo, V. Canciello, A. Orsini, M. Bernabò, N. Ancora, M. Di Federico, M. Curini, V. Mattioli, M. Russo, V. Mauro, A. Cammà, C. Barboni, B. |
author_facet | Di Lollo, V. Canciello, A. Orsini, M. Bernabò, N. Ancora, M. Di Federico, M. Curini, V. Mattioli, M. Russo, V. Mauro, A. Cammà, C. Barboni, B. |
author_sort | Di Lollo, V. |
collection | PubMed |
description | Epithelial-mesenchymal transition (EMT) is a complex biological program between physiology and pathology. Here, amniotic epithelial cells (AEC) were used as in vitro model of transiently inducible EMT in order to evaluate the transcriptional insights underlying this process. Therefore, RNA-seq was used to identify the differentially expressed genes and enrichment analyses were carried out to assess the intracellular pathways involved. As a result, molecules exclusively expressed in AEC that experienced EMT (GSTA1-1 and GSTM3) or when this process is inhibited (KLHL14 and KCNE3) were identified. Lastly, the network theory was used to obtain a computational model able to recognize putative controller genes involved in the induction and in the prevention of EMT. The results suggested an opposite role of lysophosphatidic acid (LPA) synthesis and degradation enzymes in the regulation of EMT process. In conclusion, these molecules may represent novel EMT regulators and also targets for developing new therapeutic strategies. |
format | Online Article Text |
id | pubmed-7060278 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-70602782020-03-18 Transcriptomic and computational analysis identified LPA metabolism, KLHL14 and KCNE3 as novel regulators of Epithelial-Mesenchymal Transition Di Lollo, V. Canciello, A. Orsini, M. Bernabò, N. Ancora, M. Di Federico, M. Curini, V. Mattioli, M. Russo, V. Mauro, A. Cammà, C. Barboni, B. Sci Rep Article Epithelial-mesenchymal transition (EMT) is a complex biological program between physiology and pathology. Here, amniotic epithelial cells (AEC) were used as in vitro model of transiently inducible EMT in order to evaluate the transcriptional insights underlying this process. Therefore, RNA-seq was used to identify the differentially expressed genes and enrichment analyses were carried out to assess the intracellular pathways involved. As a result, molecules exclusively expressed in AEC that experienced EMT (GSTA1-1 and GSTM3) or when this process is inhibited (KLHL14 and KCNE3) were identified. Lastly, the network theory was used to obtain a computational model able to recognize putative controller genes involved in the induction and in the prevention of EMT. The results suggested an opposite role of lysophosphatidic acid (LPA) synthesis and degradation enzymes in the regulation of EMT process. In conclusion, these molecules may represent novel EMT regulators and also targets for developing new therapeutic strategies. Nature Publishing Group UK 2020-03-06 /pmc/articles/PMC7060278/ /pubmed/32144311 http://dx.doi.org/10.1038/s41598-020-61017-y Text en © The Author(s) 2020 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/. |
spellingShingle | Article Di Lollo, V. Canciello, A. Orsini, M. Bernabò, N. Ancora, M. Di Federico, M. Curini, V. Mattioli, M. Russo, V. Mauro, A. Cammà, C. Barboni, B. Transcriptomic and computational analysis identified LPA metabolism, KLHL14 and KCNE3 as novel regulators of Epithelial-Mesenchymal Transition |
title | Transcriptomic and computational analysis identified LPA metabolism, KLHL14 and KCNE3 as novel regulators of Epithelial-Mesenchymal Transition |
title_full | Transcriptomic and computational analysis identified LPA metabolism, KLHL14 and KCNE3 as novel regulators of Epithelial-Mesenchymal Transition |
title_fullStr | Transcriptomic and computational analysis identified LPA metabolism, KLHL14 and KCNE3 as novel regulators of Epithelial-Mesenchymal Transition |
title_full_unstemmed | Transcriptomic and computational analysis identified LPA metabolism, KLHL14 and KCNE3 as novel regulators of Epithelial-Mesenchymal Transition |
title_short | Transcriptomic and computational analysis identified LPA metabolism, KLHL14 and KCNE3 as novel regulators of Epithelial-Mesenchymal Transition |
title_sort | transcriptomic and computational analysis identified lpa metabolism, klhl14 and kcne3 as novel regulators of epithelial-mesenchymal transition |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7060278/ https://www.ncbi.nlm.nih.gov/pubmed/32144311 http://dx.doi.org/10.1038/s41598-020-61017-y |
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