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TGF-β and RREB1 coordinate EMT programs in NMuMG cells

ABSTRACT: TGF-β and RREB1 coordinate EMT programs in NMuMG cells

PROVIDER: PRJNA529490 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8796440_1.fastq.gz	Fastqsanger.gz
	SRR8796440_2.fastq.gz	Fastqsanger.gz
	SRR8796433_1.fastq.gz	Fastqsanger.gz
	SRR8796433_2.fastq.gz	Fastqsanger.gz
	SRR8796434_1.fastq.gz	Fastqsanger.gz

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TGF-β and RREB1 coordinate EMT programs in NMuMG cells

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TGF-β and RREB1 coordinate EMT programs in development and cancer

Project description:Epithelial-to-mesenchymal transitions (EMT) play prominent roles during development, regeneration and tumor progression. EMTs are triggered by TGF-β, RAS and other signals that cooperatively induce the expression of master EMT transcription factors such as SNAIL. Here, we elucidate how the TGF-β and RAS pathways jointly trigger EMTs and tie them to broader developmental programs. We identify RAS response element binding protein 1 (RREB1) as a critical partner of TGF-β-activated SMAD transcription factors in driving SNAIL expression in pancreatic pre-malignant epithelial cells, lung adenocarcinoma cells, and embryonic stem cells. Moreover, SMADs and RREB1 also drive EMT-associated fibrogenic programs in epithelial cells and mesendoderm differentiation in pluripotent embryonic cells. These findings illuminate the orchestration of EMT associated programs in gastrulation, fibrosis, and cancer.

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TGF-β and RREB1 coordinate EMT programs in development and cancer

Project description:TGF-β and RREB1 coordinate EMT programs in development and cancer

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Transcription profiling of mouse mammary epithelial cells NMuMG treatd with TGF-b1 - time series experiment

Project description:Response of mouse mammary epithelial cells NMuMG to TGF-b1 - time course experiment. Identification of novel gene targets involved in TGF-b1-driven regulation of epithelial-mesenchymal transition (EMT).

2004-10-01 | E-MEXP-139 | biostudies-arrayexpress

Expression data from normal murine mammary epithelial cell line NMuMG stimulated with TGF-beta

Project description:TGF-beta is one of the most important cytokines that induce epithelial to mesenchymal transition (EMT). In this dataset, we examined TGF-beta induced changes in gene and exon level expression. Core probesets of two samples were analyzed. NMuMG cells were stimulated with TGF-beta for 24 h or left untreated.

2011-11-01 | E-GEOD-28184 | biostudies-arrayexpress

NMuMG cell response to TGF-beta and TGF-beta +2APB treatments

Project description:Recent studies demonstrate that Ca2+ signaling has an important role in EMT. Use of Ca2+ blockers such as 2APB can inhibit cell migration induced by TGF-β. Interestingly, we see an unexpected increase in Snail expression upon Ca2+ blocker treatment of both MCF10A and NMuMG cells; this increase is not observed with 2APB treatment alone. Therefore, we believe that 2APB plays a synergistic role with TGF-β in Snail induction. We propose to investigate the gene networks that change following 2APB +TGF-β treatment.

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RNA-sequencing analysis of mouse epithelial NMuMG cells with Cas9 or UGCG knock out

Project description:We report the gene expression in mouse NMuMG cells with or without UGCG depletion using RNA sequencing. After data analysis, the 11218 transcripts were identified. Among these transcripts, the TGF-β signaling target genes and EMT marker genes were significantly upregulated in UGCG depleted NMuMG cells. Then we used these genes and mouse TGF-β or EMT gene signatures to do the gene set enrichment analysis and showed the negative correlation of UGCG and TGF-β signaling or EMT in NMuMG cells.

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Gene expression in epithelial, EMT (epithelial-mesenchymal transition) and MET (mesenchymal-epithelial transition) cells

Project description:NMuMG is an epithelial cell line that can be induced into EMT by TGF-β treatment or MET by TGF-β withdrawl. During EMT, several marker genes were downregulated/upregulated, which is consistent with its mesenchymal phenotype. Transcription factors that are regulated during EMT and its reverse process MET are candidate genes for the regulations of the EMT marker genes. NMuMG cells treated with vehicle, TGF-β for 11 days, or 11days of TGF-β treatment followed by TGF-β withdrawl for another 13 days. RNA from these 3 conditions of NMuMG were extracted and subject to microarray analysis

2013-07-26 | E-GEOD-48204 | biostudies-arrayexpress

Genome-wide transcripts in NMuMG cells expressing Osr2

Project description:Analysis of NMuMG cells expressing Osr2 or treated with TGF-ß. Results provide insight into a novel function of Osr2 in EMT induction.

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LncRNA LETS1 promotes TGF--induced EMT and cancer progression

Project description:Transforming growth factor- (TGF-) signaling is a critical driver of epithelial–mesenchymal transition (EMT) and cancer progression. However, the regulatory roles of long non-coding RNAs (lncRNAs) in TGF--induced EMT and cancer progression are not well understood. Here, we identified an unannotated nuclear lncRNA LETS1 (LncRNA Enforcing TGF- Signaling 1) as a novel TGF-/SMAD target gene. Loss of LETS1 attenuates TGF--induced EMT, migration and extravasation in breast and lung cancer cells. LETS1 potentiates TGF-/SMAD signaling by stabilizing cell surface TGF- type I receptor (TRI) and thereby forms a positive feedback loop. Mechanistically, LETS1 inhibits TRI polyubiquitination by inducing the orphan nuclear receptor 4A1 (NR4A1) expression, a critical determinant of a destruction complex for inhibitory SMAD7. An unbiased interactome analysis identified the Nuclear Factor of Activated T Cells (NFAT5) as a protein partner of LETS1 to mediate activation of NR4A1 promoter. Overall, our findings characterize LETS1 as an EMT-promoting lncRNA and elucidate the mechanism by which nuclear LETS1 potentiates TGF- receptor signaling.

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