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Ras and TGF-beta signaling aggravates the metastatic and invasive potential of cancer cells through activation of the deltaNp63 alpha transcriptional program

ABSTRACT: Ras and TGF-beta signaling aggravates the metastatic and invasive potential of cancer cells through activation of the deltaNp63 alpha transcriptional program

PROVIDER: PRJNA259607 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR1559350.fastq.gz	Fastqsanger.gz
	SRR1559351.fastq.gz	Fastqsanger.gz
	SRR1559352.fastq.gz	Fastqsanger.gz
	SRR1559348.fastq.gz	Fastqsanger.gz
	SRR1559349.fastq.gz	Fastqsanger.gz

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Ras and TGF-beta signaling aggravates the metastatic and invasive potential of cancer cells through activation of the deltaNp63 alpha transcriptional program

Project description:This SuperSeries is composed of the SubSeries listed below.

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Intestinal epithelial cells transfected with Ras and treated with TGF-beta-1

Project description:RIE (rat intestinal epithelial) cells treated with 2 ng/ml of TGF-beta-1 for 1 hr were compared to control cells. The experiment was performed under identical conditions four times: RIE vs RIE - TGF-beta #1-#4. RIE-Ras cells were established by stable transfection of the parental cells with pSV2-H-Ras(12V) which contain human sequences encoding the constitutively active H-Ras(12V) protein. RIE-Ras cells treated with 2 ng/ml of TGF-beta-1 for 1 hr were compared to control cells. The experiment was performed four times under identical conditions (RIE-Ras vs RIE-RAS TGF-beta #1-#4). Keywords = TGF-beta Keywords = rat Keywords = intestinal epithelial cells Keywords: parallel sample

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

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 (RNA-Seq)

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

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TGF-β and RAS jointly unmask primed enhancers to drive metastasis (DRIPc-seq)

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

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Quantitative Proteomic Analysis in Alveolar Type II Cells Reveals the Different Capacities of RAS and TGF-β to Induce Epithelial–Mesenchymal Transition

Project description:Alveolar type II (ATII) epithelial cells function as stem cells, contributing to alveolar renewal, repair and cancer. Therefore, they are a highly relevant model for studying lung diseases, including acute injury, fibrosis and cancer, in which signals transduced by RAS and transforming growth factor (TGF)-ß play critical roles. To identify downstream molecular events following RAS and/or TGF-ß activation, we performed proteomic analysis using a quantitative label-free approach (LC-HDMSE) to provide in-depth proteome coverage and estimates of protein concentration in absolute amounts. Contact: pjss@soton.ac.uk

2021-02-04 | PXD023720 | Pride

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