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Epigenetic regulation of the mesenchymal niche during pancreatic epithelial development

ABSTRACT: Epigenetic regulation of the mesenchymal niche during pancreatic epithelial development

PROVIDER: PRJNA655909 | ENA |

REPOSITORIES: ENA

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Epigenetic regulation of the mesenchymal niche during pancreatic epithelial development

Project description:Exploring the role of epigenetic regulation in the E13.5 pancreatic mesenchyme by Eed to understand its role in chromatin regulation using ATAC-seq, transcriptional regulation using RNA-seq, and in the regulation of transcriptional heterogeneity using scRNA-seq.

2025-08-07 | GSE155875 | GEO

VPA-treatment of Panc-1-cells to study epigenetic impact mediated by histone acetylation on epithelial-mesenchymal transmission

Project description:Non-mesenchymal pancreatic cells are a potential source for cell replacement therapies aiming to restore the endocrine capacity lost during diabetes mellitus. Although a highly complex network of transcription factors underlies the differentiation, growth, and specification of pancreatic precursors, several studies indicated that the transdifferentiation of non-mesenchymal cells can be achieved by epigenetic regulation. The induction of this epithelial-mesenchymal transition through the post-translational modification of histones, exerting control over both dynamic and long-term gene expression, is a promising approach for reprogramming them into mesenchymal cells. The small molecule and histone deacetylase inhibitor valproic acid was linked to the expression of key transcription factors of pancreatic lineage in epithelial cells and insulin transcription. However, the underlying mechanisms are not fully understood. To shed further light on the potential use of valproic acid for cellular reprogramming strategies, we studied its effects on human ductal Panc-1-cells employing next generation RNA sequencing, real-time PCR and protein analysis by ELISA and western blot. Our data indicate a significant regulation of cell cycle, cell adhesion, histone acetyltransferase and metabolism-related genes, and an epithelial–mesenchymal transition through acetylation of histone H3, resulting in the phenotype of a-cells, supporting the prospect of a therapeutic usage of epithelial pancreatic cells for the purpose of reprogramming into hormonesecreting endocrine cells.

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Project description:We performed RNA-seq analysis on YFP+EpCAM+ and YFP+EpCAM- cell populations freshly isolated from three Pdx1-Cre;KrasLSL-G12D;Trp53fl/fl;Rosa26LSL-YFP (KPCY) murine pancreatic tumours. We compared the transcriptome between these two populations with the aim to understand their molecular interactions that could underlie epithelial-mesenchymal plasticity and tumour heterogeneity.

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Epigenetic landscape of HEK cells upon epithelial-to-mesenchymal transition

Project description:Epithelial-to-mesenchymal transition (EMT) allows progressive loss of epithelial traits and acquisition of mesenchymal identity promoting cell migratory and invasive properties. It is expressed by changes in gene expression program induced by changes of chromatin state and organization. To identify epigenetic landscape associated with EMT we performed chromatin immunoprecipitation (ChIP) experiments allowing nucleosome profiling (H3), distribution of histone modifications linked to actively transcribed (H3K4me3, H3K36me3 and H3K27ac) and repressed (H3K27me3) regions in epithelial (Epi) and mesenchymal (Mes) cells. These cell lines were generated by immortalization of primary HEK cells before and after naturally occured EMT.

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Erk-dependent Epigenetic Reprogramming Underlies Epithelial to Mesenchymal Transition

Project description:The series of events that allows for the conversion of adherent epithelial cells into migratory cells is collectively known as epithelial-mesenchymal transition (EMT). EMT is involved in triggering neural crest migration during development and in the pathogenesis of diseases, such as cancer metastasis. Whereas Erk signalling is known to be essential for EMT, its influence on the epigenetic and transcriptional programme underlying EMT is poorly understood. Here, using a comprehensive genome-wide analysis of H3K27ac mark and gene expression in primary mammary epithelial cells undergoing EMT, we found that Erk signalling is essential for the epigenetic reprogramming underlying hallmark gene expression and phenotypic changes of EMT. We found that the chemical inhibition of Erk signalling during EMT prevents loss and gain of H3K27ac mark at regulatory regions of epithelial and mesenchymal genes, respectively, and results in a transcriptome and epigenome closer to those of epithelial cells. Further computational analyses identified a distinct set of transcription factor motifs enriched at distal regulatory regions that are epigenetically remodelled by Erk signalling. Altogether, our study reveal an Erk-dependent epigenetic remodelling of distal regulatory elements that results in a gene expression programme that is essential for driving EMT.

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Project description:Epithelial to Mesenchymal Transition (EMT) has been associated with cancer cell heterogeneity, plasticity and metastasis. It has been the subject of several modeling effort. This logical model of the EMT cellular network aims to assess microenvironmental signals controlling cancer-associated phenotypes amid the EMT continuum. Its outcomes relate to the qualitative degrees of cell adhesions by adherent junctions and focal adhesions, two features affected during EMT. Model attractors recover epithelial, mesenchymal and hybrid phenotypes, and simulations show that hybrid phenotypes may arise through independent molecular paths, involving stringent extrinsic signals. Of particular interest, model predictions and their experimental validations indicated that: 1) ECM stiffening is a prerequisite for cells overactivating FAK-SRC to upregulate SNAIL1 and acquire a mesenchymal phenotype, and 2) FAK-SRC inhibition of cell-cell contacts through the Receptor Protein Tyrosine Phosphates kappa leads to the acquisition of a full mesenchymal rather than a hybrid phenotype.

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