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Abstract
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.
Highlights
Epithelial-mesenchymal transition (EMT) is a complex biological process
In three cultural passages, amniotic epithelial cells (AEC) spontaneously lost their cobblestone shape to acquire an elongated fibroblast-like shape
A novel putative pathway involved in the regulation of EMT process was identified by using AEC as an in vitro model
Summary
Epithelial-mesenchymal transition (EMT) is a complex biological process. intracellular pathways leading to the trans-differentiation of epithelial into fibroblastic-like cells are known, several molecular mechanisms still remain to be clarified despite the clinical urgency of the issue[1]. Regardless of the type, EMT is triggered by initiator molecules (e.g. cytokines and growth factors) able to induce the so-called EMT master regulators (Snail, Twist and Zeb, among the others) with the consequent loss of epithelial markers (primarily E-Cadherin) and the acquisition of mesenchymal ones[3]. During this transition, a number of transcriptional changes occur into epithelial cells. When cultured in the presence of P4, AEC were able to express their self-renewal ability by preserving the native epithelial phenotype that spontaneously would be lost during the in vitro expansion[26]. Revealing the underlying molecular insights of EMT in AEC becomes crucial in order to improve their use in tissue engineering protocols as well as to deepen our understanding of the intracellular pathways of this widespread biological process
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