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Identification of Smad2 and Smad3 specific binding sites in a breast cancer cell line model

ABSTRACT: We identify Smad2 and Smad3 specific binding site in a breast cancer breast cell model MDA-MB-231 using LAP-tag GFP fusion proteins under the control of endogenous regulatory elements. Stable cell lines were generated via transfection with a BAC followed by antibiotics selection. We show that LAP-fused SMad2/3 can be used to recapitulate native TGFB signaling. Smad2/Smad3 specific binding sites were identified by ChIP-seq against GFP before and after TGFB treatment. Genomic DNA was sequenced via single end sequencing on Illumina HiSeq

ORGANISM(S): Homo sapiens

PROVIDER: GSE190237 | GEO | 2021/12/08

REPOSITORIES: GEO

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Smad2 and Smad3 have differential sensitivity in relaying TGF b signaling and inversely regulate early lineage specification

Project description:The transforming growth factor beta (TGFÎ²) related signaling is one of the most important signaling pathways regulating early developmental events. Smad2 and Smad3 are structurally similar and it is mostly considered that they are equally important in mediating TGFÎ² signals. Here, we show that Smad3 is an insensitive TGFÎ² transducer as compared with Smad2. Smad3 preferentially localizes within the nucleus and is thus sequestered from membrane signaling. The ability of Smad3 in oligomerization with Smad4 upon agonist stimulation is also impaired given its unique linker region. Smad2 mediated TGFÎ² signaling plays a crucial role in epiblast development and patterning of three germ layers. However, signaling unrelated nuclear localized Smad3 is dispensable for TGFÎ² signaling-mediated epiblast specification, but important for early neural development, an event blocked by TGFÎ²/Smad2 signaling. Both Smad2 and Smad3 bind to the conserved Smads binding element (SBE), but they show nonoverlapped target gene binding specificity. We conclude that Smad2 and Smad3 possess differential sensitivities in relaying TGFÎ² signaling and have distinct roles in regulating early developmental events. GFP, GFP-Smad2 and GFP-Smad3 constitutively expressed Smad3-/- mouse ESCs were differentiated to day6 neuroepithelia and collected for Chip-Seq with an anti-GFP antibody.

2016-03-01 | E-GEOD-76557 | biostudies-arrayexpress

Smad2 and Smad3 binding sites in H345-TbRII cells

Project description:Transforming growth factor (TGF)-beta induces apoptosis of many types of cancer cells and acts as a tumor suppressor. We found lower expression of TGF-beta type II receptor (TbRII) in most of SCLC cells and tissues than in normal lung epithelial cells and normal lung tissues, respectively. In vitro cell growth and in vivo tumor formation were suppressed by TGF-beta-mediated apoptosis when the wild-type TbRII was overexpressed in SCLC cells. We therefore determined Smad2 and Smad3 (Smad2/3) binding sites in a SCLC cell line H345 stably expressing exogenous TbRII (H345-TbRII) to identify target genes of TGF-beta. Smad2 and Smad3 binding sites in H345-TbRII cells were determined by ChIP-seq (one sample analysis, without replicates).

2015-09-15 | E-GEOD-63871 | biostudies-arrayexpress

Differential effects of Smad2 and Smad3 in regulation of macrophage phenotype and function in the infarcted myocardium

Project description:TGF-βs regulate macrophage responses, by activating Smad2/3. We have previously demonstrated that macrophage-specific Smad3 stimulates phagocytosis and mediates anti-inflammatory macrophage transition in the infarcted heart. However, the role of macrophage Smad2 signaling in myocardial infarction remains unknown. We studied the role of macrophage-specific Smad2 signaling in the healing infarct, and we explored the basis for the distinct effects of Smad2 and Smad3. Infarct macrophages exhibited both Smad2 and Smad3 activation. In contrast to the effects of Smad3 loss, myeloid cell-specific Smad2 disruption had no effects on mortality, ventricular dysfunction and adverse remodeling, after myocardial infarction. Phagocytic removal of dead cells, macrophage and myofibroblast infiltration, collagen deposition, angiogenesis and scar remodeling were not affected by macrophage Smad2 loss. In isolated macrophages, TGF-β1, -β2 and -β3, activated both Smad2 and Smad3, whereas BMP6 triggered only Smad3 activation. Smad2 and Smad3 had similar patterns of nuclear translocation in response to TGF-β1. Smad3, and not Smad2, was the main mediator of transcriptional effects of TGF-β on macrophages and Smad3 loss resulted in enrichment of genes associated with RAR/RXR signaling, cholesterol biosynthesis and lipid metabolism. In conclusion, the in vivo and in vitro effects of TGF-β on macrophage function involve Smad3, and not Smad2.

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Smad2 and Smad3 have differential sensitivity in relaying TGF b signaling and inversely regulate early lineage specification

Project description:The transforming growth factor beta (TGFβ) related signaling is one of the most important signaling pathways regulating early developmental events. Smad2 and Smad3 are structurally similar and it is mostly considered that they are equally important in mediating TGFβ signals. Here, we show that Smad3 is an insensitive TGFβ transducer as compared with Smad2. Smad3 preferentially localizes within the nucleus and is thus sequestered from membrane signaling. The ability of Smad3 in oligomerization with Smad4 upon agonist stimulation is also impaired given its unique linker region. Smad2 mediated TGFβ signaling plays a crucial role in epiblast development and patterning of three germ layers. However, signaling unrelated nuclear localized Smad3 is dispensable for TGFβ signaling-mediated epiblast specification, but important for early neural development, an event blocked by TGFβ/Smad2 signaling. Both Smad2 and Smad3 bind to the conserved Smads binding element (SBE), but they show nonoverlapped target gene binding specificity. We conclude that Smad2 and Smad3 possess differential sensitivities in relaying TGFβ signaling and have distinct roles in regulating early developmental events.

2016-03-01 | GSE76557 | GEO

Smad2 and Smad3 binding sites in H345-TbRII cells

2015-09-15 | GSE63871 | GEO

The phosphorylation of the Smad2/3 linker region by Nemo-like kinase regulates TGF-β signaling

Project description:Smad2 and Smad3 (Smad2/3) primarily mediates the transforming growth factor-β (TGF-β) signaling that drives cell proliferation, differentiation, and migration. The dynamics of the Smad2/3 phosphorylation provides the key mechanism for regulating the TGF-β signaling pathway. Here we identified NLK as a novel regulator of TGF-β signaling pathway via modulating the phosphorylation of Smad2/3 in the linker region.

2021-09-10 | PXD023957 | Pride

SMAD2/3 binding pattern in triple-negative breast cancer cell lines, Hs578T and BT549 [ChIP-seq]

Project description:SMAD2 and SMAD3 have diverse binding profiles in triple-negative breast cancer cell lines.

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RNAi profiling by array of of Smad2 and Smad3 in mouse mammary epithelial cells treated with TGF-beta to induce epithelial-to-mesenchymal transition

Project description:Effects of Smad3 and Smad2 knock-down on TGFbeta-induced epithelial-to-mesenchymal transition (EMT) in mouse mammary epithelial (Nme) cells

2009-04-01 | E-MEXP-1342 | biostudies-arrayexpress

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

2006-11-14 | GSE6242 | GEO

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Project description:To dissected the roles of SMAD2/3 and SMAD4 in mouse embryonic stem cells (mESC), knockouts of SMAD2/3 (SMAD2 and SMAD3 double knockout, S2/3DKO) and SMAD4 (SMAD4 knockout, S4KO) were used to conduct RNAseq in ES and EB conditions.

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