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

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE205911 | GEO | 2024/06/01

REPOSITORIES: GEO

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

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 colonic epithelia cells derived from DSS treatment.

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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-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

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

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

| PRJNA848221 | 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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Gene expression analyses of SMAD4 knockdown in pancreatic cell line

Project description:The transforming growth factor β (TGF-β) signaling protein SMAD4 is lost in 60% of PDAC, and this has been associated with poorer prognosis. We expressed SMAD4 in human PDAC cell lines BxPC3, by selection of stable clones containing an inducible SMAD4 Tet-ON construct. After 24h of SMAD4 expression, TGF-β signaling-dependent G1-arrest was observed in BxPC3 cells with an increase in the G1-phase fraction from 48.9% to 71.5%. Microarray analysis of gene expression at 8h, 24h, and 48h after SMAD4 expression characterized the regulatory impact of SMAD4 expression in a SMAD4-null PDAC cell line and identified novel targets of TGF-β signaling.

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

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SMAD4 plays acritical role in CD8 T cell cytotoxic function [RNA-seq]

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