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Genome-wide maps of chromatin state in cultured male germline stem cells [scATAC-seq]

ABSTRACT: We report the application of single-cell ATAC-seq to reconstruct the epigenetic program and identify key transcription factors and cis-regulatory elements associated with the epithelial and mesenchymal heterogeneity and G9a inhibition in cultured male germline stem cells (GSCs). First, we identified epithelial-like and mesenchymal-like clusters in the sample. Pseudotime trajectory also indicated that GSCs could undergo EMT-like process with unique regulators in different stages. Lastly, we showed that G9a inhibition could suppress the EMT-like process in GSCs.

ORGANISM(S): Mus musculus

PROVIDER: GSE159414 | GEO | 2023/07/01

REPOSITORIES: GEO

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Gene expression and chromatin accessibility profiles of cultured male germline stem cells [RNA-seq and ATAC-seq]

Project description:We report the application of RNA-seq to profile the transcriptome associated with Oct4-GFP intensity, feeder v.s. feeder-free culture, epithelial and mesenchymal heterogeneity and G9a inhibition in cultured male germline stem cells (GSCs). First, we confirmed that the self-renewal gene expression levels of feeder culture and feeder-free culture were comparable to each other. Next, we investigatied the transcriptional differences among GSCs with different Oct4-GFP intensity. Then, we explored the transcriptonal differences between epithelial-like and mesenchymal-like GSCs, demonstrating GSCs could undergo an EMT-like process. Lastly, we showed that G9a inhibition could suppress the EMT-like process in GSCs.

2023-07-01 | GSE159412 | GEO

Selvaggio2020 - Microenvironment control of hybrid Epithelial-Mesenchymal phenotypes

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.

2020-06-30 | MODEL2004040001 | BioModels

Regan2022 - Mechanosensitive EMT model

Project description:This file contains a 136-node modular Boolean network model of EMT triggered by biomechanical and growth signaling crosstalk, linked to a published network of epithelial contact inhibition, proliferation, and apoptosis (MODEL2006170001). This model reproduces the ability of the core EMT transcriptional network to maintain distinct epithelial, hybrid E/M and mesenchymal states, as well as EMT driven by mitogens such as EGF on stiff ECM. We also reproduce the observed lack of stepwise MET, in that our model's dynamics does not pass through the hybrid E/M state during MET. We show that in the absence of strong autocrine signals such as TGFβ (not included in this version), cells cannot maintain their mesenchymal state in the absence of mitogens, on softer matrices, or at high cell density.

2023-12-13 | MODEL2208050001 | BioModels

Regan2022 - Mechanosensitive EMT model with autocrine TGFbeta signaling

Project description:This model is an expansion of the Regan2022 - Mechanosensitive EMT model (MODEL2208050001); it includes a TGFβ signaling module and autocrine signaling in mesenchymal cells. The expanded 150-node (630 link) modular model undergoes EMT triggered by biomechanical and growth signaling crosstalk, or by TGFβ. As its predecessor, this model also reproduces the ability of the core EMT transcriptional network to maintain distinct epithelial, hybrid E/M and mesenchymal states, as well as EMT driven by mitogens such as EGF on stiff ECM. We also reproduce the observed lack of stepwise MET, in that our model's dynamics does not pass through the hybrid E/M state during MET. We show that in the absence of strong autocrine signals such as TGFβ (not included in this version), cells cannot maintain their mesenchymal state in the absence of mitogens, on softer matrices, or at high cell density. In contrast, potent autocrine signaling can stabilize the mesenchymal state in all but very dense monolayers on soft ECM. This expanded model also reproduces the inhibitory effects of TGFβ on proliferation and anoikis resistance in mesenchymal cells, as well as its ability to trigger apoptosis on soft ECM vs. EMT on stiff matrices. The model offers several experimentally testable predictions related to the effect of neighbors on partial vs. full EMT, the tug of war between mitosis and the maintenance of migratory hybrid E/M states, as well as cell cycle defects in dynamic, heterogeneous populations of epithelial, hybrid E/M and mesenchymal cells.

2023-12-13 | MODEL2208050002 | BioModels

Epithelial to mesenchymal transition shed microvesicle proteome

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2021-03-18 | PXD022290 | Pride

Gene Transcriptional Variation of Hepatic Progenitor Cells after TGF- 1-Induced EMT Transition and EGF-Induced MET Reversion

Project description:TGF-b1 induces hepatic progenitor cells experience an epithelial-mesenchymal transition, and EGF could reverse this process via mesenchymal-epithelial transition. Yet, the mechanism underline these EMT and MET processes are not clear. The aim of this study is to reveal the genes with significant difference during these EMT and MET process in hepatic progenitor cells.

2021-04-23 | GSE165858 | GEO

Cellular and extracellular vesicle RNA sequence for E-cadherin-RFP EMT reporter system expressing mouse breast cancer cell line Py2T during EMT/MET

Project description:Epithelial-mesenchymal transition (EMT) is a process by which epithelial cells lose cell-cell contact and gain cancer malignancy such as invasion, stemness, chemoresistance and metastasis. Reverse precess, mesenchymal-epithelial transition (MET) is also important for colonization. Extracellular vesicles (EVs) secreted from cancer cells are also important for cancer malignancy. To analyze RNAs from cells and EVs during EMT and MET, RNA sequencing was performed using E-cadherin-RFP/Py2T reporter system.

2020-12-31 | E-MTAB-9750 | biostudies-arrayexpress

"High Levels of EMT-TFs for the Diagnosis of Colorectal Cancer (CRC)"

Project description:The present study is aimed at detecting and measuring mRNA levels of genes involved in epithelial to mesenchymal transition (EMT) in biological samples, i.e. in peripheral blood samples of colorectal cancer (CRC) patients and healthy controls, to determine the presence of disease, its progression and risk of recurrence.

| 2334276 | ecrin-mdr-crc

Transcriptome of EMT induced MCF10A cells by TGFb treatment or SNAIL S6A expression.

Project description:EMT, Epithelial to mesenchymal transition is a developmental biology process associated with migration, known to be involved in cancer metastasis. To study this process, we used the breast epithelial cell line MCF10A that enter in EMT after treatment with the cytokine TGFB or by expression of EMT transcriptor factor SNAIL.

2017-01-30 | GSE89152 | GEO

SWI/SNF Chromatin-Remodeling Factor Smarcd3/Baf60c Controls Epithelial-Mesenchymal Transition by Inducing Wnt5a Signaling

Project description:We previously identified a gene signature predicted to regulate the epithelial-mesenchymal transition (EMT) in both epithelial tissue stem cells and breast cancer cells. A phenotypic RNA interference (RNAi) screen identified the genes within this 140-gene signature that promoted the conversion of mesenchymal epithelial cell adhesion molecule-negative (EpCAM-) breast cancer cells to an epithelial EpCAM+/high phenotype. The screen identified 10 of the 140 genes whose individual knockdown was sufficient to promote EpCAM and E-cadherin expression. Among these 10 genes, RNAi silencing of the SWI/SNF chromatin-remodeling factor Smarcd3/Baf60c in EpCAM- breast cancer cells gave the most robust transition from the mesenchymal to epithelial phenotype. Conversely, expression of Smarcd3/Baf60c in immortalized human mammary epithelial cells induced an EMT. The mesenchymal-like phenotype promoted by Smarcd3/Baf60c expression resulted in gene expression changes in human mammary epithelial cells similar to that of claudin-low triple-negative breast cancer cells. These mammary epithelial cells expressing Smarcd3/Baf60c had upregulated Wnt5a expression. Inhibition of Wnt5a by either RNAi knockdown or blocking antibody reversed Smarcd3/Baf60c-induced EMT. Thus, Smarcd3/Baf60c epigenetically regulates EMT by activating WNT signaling pathways. sampleXreference

2013-08-19 | E-GEOD-40145 | biostudies-arrayexpress

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