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Smad4 restricts injury-provoked biliary proliferation and carcinogenesis (AKPS_EV_vs_Smad4_MethylSeq)

ABSTRACT: Reduced representation bisulfite sequencing (RRBS) on the same TGFβ-treated AKPS lines (with EV or Smad4) revealed that Smad4 impacts DNA methylation (DNAme), with decreases in intergenic DNAme as the most impacted in our CCA models.

ORGANISM(S): Mus musculus

PROVIDER: GSE237680 | GEO | 2023/12/07

REPOSITORIES: GEO

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Smad4 restricts injury-provoked biliary proliferation and carcinogenesis (AKPS_EV_vs_Smad4_RNAseq)

Project description:RNA-sequencing of TGFβ treated empty vector (EV) or Smad4-expressing AKPS lines followed by GSEA revealed a number of gene sets overlapping with those obtained from analyses in reactive cholangiocytes. Hallmark gene sets MYC, E2F, G2M checkpoint, and oxidative phosphorylation were enriched with loss of Smad4, while TGFβ signaling, EMT, and TNFα were enriched with intact Smad4 signaling, suggesting conserved growth suppressive functions of Smad4 in primary cholangiocytes and advanced cancer.

2023-12-07 | GSE237679 | GEO

Smad4 restricts injury-provoked biliary proliferation and carcinogenesis (Smad4_floxed_vs_WT_RNAseq)

Project description:To understand the processes regulated by Smad4 in reactive cholangiocytes, Ctl and Smad4del mice were provided DDC diet for 2 weeks after which reactive cholangiocytes were isolated from digested injured mouse liver via FACS followed by RNA amplification and sequencing analysis. Gene set enrichment analysis of Smad4-perturbed reactive cholangiocytes implicates Smad4 in proliferative, metabolic, and inflammatory pathways.

2023-12-07 | GSE237678 | GEO

Smad4 restricts injury-provoked biliary proliferation and carcinogenesis

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

2023-12-07 | GSE237681 | GEO

Gene expression analyses of SMAD4 knockdown in pancreatic cell line

Project description:The transforming growth factor ? (TGF-?) 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-? 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-? signaling. We used BxPC3 cells infected by pINDCUER-SMAD4-Puro virus. After 24h, 1µg/ml doxycycline was added to experimental wells. We profiled the gene expression after 8hr, 24hr and 48hr treatment with doxycycline as well as control at 8hr.

2015-08-20 | E-GEOD-70940 | biostudies-arrayexpress

Expression data from Smad4-siRNA bEnd3 cells

Project description:TGF-beta/Smads signaling plays important roles in vascular integrity. To identify potential Smad4 target genes in brain endothelial cells that control cerebrovascular integrity, the microarray assay was performed to compare the gene expression profiles of bEnd3 transfected with Smad4-siRNA and control-siRNA. bEnd3 cells were infected by Smad4-siRNA or control-siRNA retrovirus particles produced by PLAT-E packaging cells and selected by puromycin. The specific and control RNAi cells were used for RNA extraction and hybridization on Affymetrix microarrays. Two independent infections were performed and samples were pooled in order to obtain representative populations.

2011-04-17 | E-GEOD-15736 | biostudies-arrayexpress

Gene expression profile in platelets of mouse regulated by Smad4 gene

Project description:Mutations of SMAD family member 4 (Smad4) gene caused Hereditary Hemorrhagic Telangiectasia (HHT). It was believed that bleeding disorders were caused by arteriovenous malformation in this syndrome. Although several studies indicated dysfunction of platelets from HHT patient, the role(s) of smad4 in platelet function has not been examined. In this study, using megakaryocyte/platelet-specific Smad4-deficient mice, we investigated the physiological function of Smad4 in platelet activation and the underlying mechanism. Microarray data demonstrated that the level of mRNA for multiple genes changed in Smad4 deficient platelet. For microarray analysis, total mRNA was extracted from washed platelets from Smad4f/f or Smad4M-bM-^HM-^R/M-bM-^HM-^R mice (for each group, n=6). mRNA was labeled and hybridized to Affymetrix Mouse Genome 430 2.0 chips according to manufacturer's instructions (Affymetrix).

2013-01-29 | E-GEOD-43814 | biostudies-arrayexpress

Smad4 and Trim33 dependend nodal/activin responsive genes in differentiated mouse ESCs

Project description:In differentiated mouse ESCs, most of the nodal/activin responsive genes are dependent on both Smad4 and Trim33, some are solely dependent on Smad4, and some are dependent on Trim33. Ebs at Day2.5 from WT, Smad4 null, and Trim33 knock-down ESCs, were treated with activin or SB 431542 for 2 h.

2012-01-09 | E-GEOD-32903 | biostudies-arrayexpress

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.

2015-08-20 | GSE70940 | GEO

SMAD4 represses FOSL1 expression and pancreatic cancer metastatic colonization

Project description:Less than 8% of patients diagnosed with pancreatic ductal adenocarcinomas (PDAC) survive more than five years in part due to late stage diagnosis. Approximately half of PDAC patients exhibit loss of SMAD4, which correlates with increased metastatic disease. Here we demonstrate that SMAD4 is a suppressor of metastatic colonization. Using isogenic human PDAC cell lines expressing or lacking SMAD4, both in vitro and in vivo, we define SMAD4-dependent gene expression changes in metastatic lesions. We performed a pooled in vivo open reading frame (ORF) screen of SMAD4 transcriptional targets and identified genes that, induce tumor seeding and growth at secondary sites. We found that expression of the transcription factor FOSL1 was sufficient to drive metastatic colonization. SMAD4 directly binds and represses the activity of the FOSL1 enhancer. These studies demonstrate a direct role for SMAD4 in regulating metastatic colonization and identify FOSL1 as a SMAD4-regulated gene involved in PDAC progression.

2021-08-02 | GSE148248 | GEO

Transcription profiling of human mammary epithelial cell line MDA-MB-468 acking endogenous Smad4 nfected with either an adenovirus carrying GFP cDNA (control) or Smad4 cDNA (to restore the Smad4 activity in the cells). Cells were treated with TGF-b1 (0.5 ng/ml) or BMP-7 (300 ng/ml) for 2 or 12h

Project description:Identification of novel TGF-b1 and BMP-7-regulated genes in epithelial cells.<br> <br> Human mammary epithelial cell line MDA-MB-468 that is lacking endogenous Smad4 was infected with either an adenovirus carrying GFP cDNA (control) or Smad4 cDNA (to restore the Smad4 activity in the cells). Cells were treated with TGF-b1 (0.5 ng/ml) or BMP-7 (300 ng/ml) for 2 or 12h. Smad4-independent vs Smad4-dependent response was measured. Also response to both growth factors was compared.

2004-03-15 | E-MEXP-78 | biostudies-arrayexpress

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