Dynamics of chromatin accessibility during TGF-beta-induced EMT of Ras-transformed mammary gland epithelial cells
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA285342 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR5001350.fastq.gz | Fastqsanger.gz | |||
| SRR5001360.fastq.gz | Fastqsanger.gz | |||
| SRR5001370.fastq.gz | Fastqsanger.gz | |||
| SRR5001380.fastq.gz | Fastqsanger.gz | |||
| SRR5001361.fastq.gz | Fastqsanger.gz |
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Project description:We performed global mapping of accessible chromatin in mouse mammary gland epithelial EpH4 cell line and its Ras-transformed derivative (EpRas) using formaldehyde-assisted isolation of regulatory element (FAIRE)-sequencing (seq) to analyze the mechanisms of transcriptional regulation during TGF-beta-induced EMT.
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Project description:This SuperSeries is composed of the SubSeries listed below. Epithelial-mesenchymal transition (EMT) is induced by transforming growth factor (TGF)-beta stimulation and facilitates tumor progression. We here performed global mapping of accessible chromatin in the mouse mammary gland epithelial EpH4 cell line and its Ras-transformed derivative (EpRas) using formaldehyde-assisted isolation of regulatory element (FAIRE)-sequencing (seq). We also searched for differentially expressed transcription factors by RNA-seq and found that Etv4, an ETS family oncogenic transcription factor, was strongly expressed in EpRas cells. Moreover, chromatin immunoprecipitation (ChIP)-seq showed that Etv4 bound to more than one-third of the accessible chromatin regions in EpRas cells treated with TGF-beta. We found by gene ontology analysis that genes encoding extracellular proteins are the most strongly down-regulated genes by Etv4 and Etv5 siRNAs. These findings suggest a mechanism of transcriptional regulation during TGF-beta-induced EMT that involves alterations of accessible chromatin.
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Project description:We performed global mapping of accessible chromatin in mouse mammary gland epithelial EpH4 cell line and its Ras-transformed derivative (EpRas) using formaldehyde-assisted isolation of regulatory element (FAIRE)-sequencing (seq) to analyze the mechanisms of transcriptional regulation during TGF-beta-induced EMT.
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Project description:Epithelial-mesenchymal transition (EMT) is induced by transforming growth factor (TGF)-? and facilitates tumor progression. We here performed global mapping of accessible chromatin in the mouse mammary gland epithelial EpH4 cell line and its Ras-transformed derivative (EpRas) using formaldehyde-assisted isolation of regulatory element (FAIRE)-sequencing. TGF-? and Ras altered chromatin accessibility either cooperatively or independently, and AP1, ETS, and RUNX binding motifs were enriched in the accessible chromatin regions of EpH4 and EpRas cells. Etv4, an ETS family oncogenic transcription factor, was strongly expressed and bound to more than one-third of the accessible chromatin regions in EpRas cells treated with TGF-?. While knockdown of Etv4 and another ETS family member Etv5 showed limited effects on the decrease in the E-cadherin abundance and stress fiber formation by TGF-?, gene ontology analysis showed that genes encoding extracellular proteins were most strongly down-regulated by Etv4 and Etv5 siRNAs. Accordingly, TGF-?-induced expression of Mmp13 and cell invasiveness were suppressed by Etv4 and Etv5 siRNAs, which were accompanied by the reduced chromatin accessibility at an enhancer region of Mmp13 gene. These findings suggest a mechanism of transcriptional regulation during Ras- and TGF-?-induced EMT that involves alterations of accessible chromatin, which are partly regulated by Etv4 and Etv5.
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Project description:Epithelial-to-mesenchymal transitions (EMTs) and extracellular matrix (ECM) remodeling are distinct yet important processes during carcinoma invasion and metastasis. TGF-β and RAS, signaling through SMAD and RAS-responsive element-binding protein 1 (RREB1), jointly trigger expression of EMT and fibrogenic factors as two discrete arms of a common transcriptional response in carcinoma cells. Here we demonstrate that both arms form a program for lung adenocarcinoma pulmonary metastasis and identify chromatin determinants tying the expression of the constituent genes to TGF-β and RAS dual inputs. RREB1 binds near H4K16ac histone marks and histone H2A.Z-loaded nucleosomes at enhancers in the fibrogenic genes IL11, PDGFB, and HAS2 and the EMT transcription factor SNAI1, priming these enhancers for activation by a SMAD4-INO80 nucleosome remodeling complex in response to TGF-β. These regulatory properties set the fibrogenic EMT program apart from RAS-independent TGF-β gene responses and illuminate the operation and vulnerabilities of a transcriptional program that promotes metastatic outgrowth.
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