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TGF-β promotes colitis and cancer development in Smad4-deficient intestinal epithelium in a Yap-dependent manner (organoids)

ABSTRACT: TGF-β promotes colitis and cancer development in Smad4-deficient intestinal epithelium in a Yap-dependent manner (organoids)

PROVIDER: PRJNA848221 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19631300_1.fastq.gz	Fastqsanger.gz
	SRR19631300_2.fastq.gz	Fastqsanger.gz
	SRR19631301_1.fastq.gz	Fastqsanger.gz
	SRR19631301_2.fastq.gz	Fastqsanger.gz
	SRR19631302_1.fastq.gz	Fastqsanger.gz

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TGF-β promotes colitis and cancer development in Smad4-deficient intestinal epithelium in a Yap-dependent manner (organoids)

Project description:TO highlight an integral role of the TGF-β/Smad4 axis in restraining intestinal inflammation and suggest TGF-β or Yap signaling as potential therapeutic targets in inflammatory bowel disease patients with decreased Smad4 expression. We then performed gene expression profiling analysis using data obtained from RNA-seq of indicated intestinal organoids.

2024-06-01 | GSE205911 | GEO

TGF-β promotes colitis and cancer development in Smad4-deficient intestinal epithelium in a Yap-dependent manner (DSS)

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TGF-β promotes colitis and cancer development in Smad4-deficient intestinal epithelium in a Yap-dependent manner

Project description:TGF-β promotes colitis and cancer development in Smad4-deficient intestinal epithelium in a Yap-dependent manner

| PRJNA848220 | ENA

TGF-β promotes colitis and cancer development in Smad4-deficient intestinal epithelium in a Yap-dependent manner (DSS)

Project description:TGF-β promotes colitis and cancer development in Smad4-deficient intestinal epithelium in a Yap-dependent manner (DSS)

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TGF-beta-independent function of SMAD4 preconditions naïve CD8 T-cells to prevent severe microbiota-driven chronic intestinal inflammation [RNAseq]

Project description:SMAD4, a key mediator of TGF-beta signaling, plays a crucial role in T cells to prevent chronic intestinal inflammation through unknown mechanisms. We reveal that SMAD4 in CD8 T cells prevents chronic intestinal inflammation primarily in a TGF-beta-independent manner. Mechanistically, SMAD4, in CD8 T cells, acts as a basal and tonic repressor of TGF-beta-target genes at the transcriptional and epigenetic level, prior to any TGF-beta signal. SMAD4 deletion affects aberrantly a wide range of TGF-beta-target genes, thereby promoting accumulation and epithelial retention of CD8.alpha.beta T cells inversely to total TGF-beta signaling disruption. Moreover, SMAD4 deletion unleashes the expression of TGF-beta-signaling-repressors and hampers TGF-β-mediated CD8 T cell immunosuppression, eliciting their chronic activation. Hence, in a feedforward mechanism, SMAD4 both blocks the TGF-beta signature in CD8 T cells and pre-sensitizes them to TGF-beta.

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TGF-beta-independent function of SMAD4 preconditions naïve CD8 T-cells to prevent severe microbiota-driven chronic intestinal inflammation [ChIPseq]

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DACH1 inhibits TGF-beta signaling through binding Smad4

Project description:The vertebrate homologues of Drosophila dachsund, DACH1 and DACH2, have been implicated as important regulatory genes in development. DACH1 plays a role in retinal and pituitary precursor cell proliferation and DACH2 plays a specific role in myogenesis. DACH proteins contain a domain (DS-domain) that is conserved with the proto-oncogenes Ski and Sno. Since the Ski/Sno proto-oncogenes repress AP-1 and SMAD signaling, we hypothesized that DACH1 might play a similar cellular function. Herein, DACH1 was found to be expressed in breast cancer cell lines and to inhibit TGF-beta induced apoptosis. DACH1 repressed TGF-beta induction of AP-1 and Smad signaling in gene reporter assays and repressed endogenous TGF-beta responsive genes by microarray analyses. DACH1 bound to endogenous NCoR and Smad4 in cultured cells and DACH1 co-localized with NCoR in nuclear dot-like structures. NCoR enhanced DACH1 repression and the repression of TGF-beta-induced AP-1 or Smad-signaling by DACH1 required the DACH1 DS domain. The DS-domain of DACH was sufficient for NCoR-binding at a Smad4-binding site. Smad4 was required for DACH1 repression of Smad signaling. In Smad4 null HTB-134 cells, DACH1 inhibited the activation of SBE-4 reporter activity induced by Smad2 or Smad3 only in the presence of Smad4. DACH1 participates in the negative regulation of TGF-beta signaling by interacting with NCoR and Smad4. Keywords: other

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MDA-MB-468 Smad4 positive/negative clones treated with TGF-ß

Project description:By performing oligonucleotide microarray analysis the role of Smad4 in response to TGF-ß was evaluated in established MDA-MB-468 Smad4 negative and positive clones that were treated with TGF-ß for different time points. Keywords: time-course

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Identification of the gene transcription mediated by TGF-β-Smad2/3-Smad4 signaling

Project description:TGF-β signaling is known to be very much dependent on the formation of Smad2/3-Smad4 transcription regulatory complexes. However, the signaling functions of Smad2/3-Smad4 in TGF-β-induced responses are obscure as TGF-β also initiates a number of other signaling pathways. In this study, we systematically assessed the contribution of TGF-β-Smad2/3-Smad4 signaling to target gene transcription. Individual Smads were selectively knocked down in Hep3B cells by stable RNA interference (RNAi). We identified TGF-β-responsive genes using genome-wide oligonucleotide microarrays and confirmed their dependency on Smad2, Smad3 or Smad4 by the combination of RNAi and microarray assay. The major finding from our microarray analysis was that of the 2039 target genes seen to be regulated via TGF-β induction, 190 were differentially transcriptionally controlled by Smad2-Smad4 and Smad3-Smad4 signaling and the latter control mechanism appeared to be functionally more important. We also found evidence of competition between Smad2 and Smad3 for their activation when controlling the transcription of target genes. Keywords: cell type comparison

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TGF-β promotes colitis and cancer development in Smad4-deficient intestinal epithelium in a Yap-dependent manner

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

2024-06-01 | GSE205912 | GEO