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TGF-β and RAS jointly unmask primed enhancers to drive metastasis (ATAC-Seq)

ABSTRACT: TGF-β and RAS jointly unmask primed enhancers to drive metastasis (ATAC-Seq)

PROVIDER: PRJNA1077391 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27996700_1.fastq.gz	Fastqsanger.gz
	SRR27996700_2.fastq.gz	Fastqsanger.gz
	SRR27996701_1.fastq.gz	Fastqsanger.gz
	SRR27996701_2.fastq.gz	Fastqsanger.gz
	SRR27996702_1.fastq.gz	Fastqsanger.gz

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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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TGF-β and RAS jointly unmask primed enhancers to drive metastasis (Mnase-Seq)

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