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TGFB signaling effect on cultured NHLF cells

ABSTRACT: TGFβ activates a signal transduction cascade that results in the microRNAs and genes transcription. The objective of this study is to identify miRNAs which are regulated through TGFB signaling pathway

ORGANISM(S): Homo sapiens

PROVIDER: GSE27156 | GEO | 2013/01/04

SECONDARY ACCESSION(S): PRJNA137393

REPOSITORIES: GEO

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TGFB signaling effect on cultured NHLF cells

Project description:TGFβ activates a signal transduction cascade that results in the microRNAs and genes transcription. The objective of this study is to identify miRNAs which are regulated through TGFB signaling pathway Cultured NHLF cells at 30-50% confluence were treated with 5 ng/mL TGFB1 or DMSO.

2013-01-04 | E-GEOD-27156 | biostudies-arrayexpress

SMAD3 targets in A549 lung epithelial cells

Project description:TGFβ activates a signal transduction cascade that results in the transcription of genes, primarily through the DNA-binding transcription factor SMAD3. The objective of this study is to identify SMAD3 binding targets and the molecular pathways affected by the TGFβ1/SMAD3 signal transduction on a genome-wide scale.

2011-06-24 | GSE26858 | GEO

Transcriptomic Analysis of Differentiating Primary Myoblasts treated or not with TGFB1 recombinant protein or ITD-1 compound.

Project description:Transforming Growth Factor beta (TGFβ) signaling cascade plays a fundamental role during muscle development and regeneration. Previous reports proposed several roles for the TGFβ superfamily members and generally they are considered negative regulators of myogenic differentiation. However, the activation of this signaling pathway has been shown to be essential to obtain a correct muscle tissue repair process. Due to these contrasting results, we decided to investigate the role of TGFb cascade in muscle cells. To identify the genetic networks regulated by TGFB signaling in muscle cells, we performed transcriptome analysis of differentiated primary myocytes, stimulated with either TGFB1 or ITD-1

2019-10-01 | GSE123425 | GEO

Hepatocyte-controlled availability of activated TGFb reprograms macrophage polarization affecting liver injury and regeneration

Project description:We describe a distinct macrophage population, whose presence in the liver during homoeostasis depends on recruitment signals mediated by the chemokine receptor CCR2. The identified polarization state of this population closely resembles that induced in co-culture experiments, where hepatocytes are reducing the availability of TGFb to macrophages. Accordingly, disruption of TGFb signal transduction in macrophages phenocopies the influence of hepatocytes on macrophage polarization.

2022-12-31 | E-MTAB-11727 | biostudies-arrayexpress

SMAD3 targets in A549 lung epithelial cells

Project description:TGF? activates a signal transduction cascade that results in the transcription of genes, primarily through the DNA-binding transcription factor SMAD3. The objective of this study is to identify SMAD3 binding targets and the molecular pathways affected by the TGF?1/SMAD3 signal transduction on a genome-wide scale. Cultured A549 cells at 30-50% confluence were treated with 10 uM SIS3 in dimethyl sulfoxide (DMSO), or DMSO (vehicle-only) 30 min prior to TGF?1 treatment. Cells were treated with 2 ng/mL recombinant TGF?1 for 0, 2, 12, and 24 h.

2011-06-24 | E-GEOD-26858 | biostudies-arrayexpress

TGFb dependent Treg conversion and the inhibition of conversion by IL6

Project description:Analysis of CD4+ cells activated with anti-CD3 and cultured in the presence of IL2. The effects of TGFb and IL6 on Treg conversion were analyzed to discover methods of inhibiting Treg conversion and/or Treg functional inhibition. CD4+ T-cells were enriched from lymph nodes of Foxp3-GFP mice and cultured under the under the following conditions: 1) anti-CD3+IL2; 2) anti-CD3+IL2+TGFβ; 3) anti-CD3+IL2+TGFβ+IL6; and 4) anti-CD3+IL2+IL6. On day 4 cells were collected, stained with anti-CD4-PE, and sorted into CD4+FOXP3- and CD4+FOXP3+ populations (>95% purity). For each treatment condition T-effector cells and Tregs were labeled independently (either cy3 or cy5) and hybridized together for a two-color array experiment. Each treatment condition had dye swapped replicates, and a minimum of 3 replicate in total.

2010-03-25 | GSE21027 | GEO

MicroRNA profiling of human stomach cancer, gastritis and normal stomach tissue shows that MicroRNAs regulated by E2F1 affect TGFb-dependent cell cycle arrest and apoptosis

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2008-03-01 | E-TABM-434 | biostudies-arrayexpress

PHF13 Activates Enhancers to Promote TGFb-Induced Epithelial-to-Mesenchymal Transition

Project description:PHF13 Activates Enhancers to Promote TGFb-Induced Epithelial-to-Mesenchymal Transition

| PRJNA692160 | ENA

Hepsin promotes breast tumor growth signaling via the TGFb-EGFR axis

Project description:Hepsin, a type II transmembrane serine protease, is commonly overexpressed in prostate and breast cancer. The hepsin protein is stabilized by the Ras-MAPK pathway, and downstream, this protease regulates the degradation of extracellular matrix components and activates growth factor pathways, such as hepatocyte growth factor and transforming growth factor beta (TGFβ) pathway. However, how exactly active hepsin promotes cell proliferation machinery to sustain tumor growth is not fully understood. Here, we show that genetic deletion of Hpn in a WAP-Myc model of aggressive MYC-driven breast cancer inhibits tumor growth in the primary syngrafted sites and the growth of disseminated tumors in the lungs. The suppression of tumor growth upon loss of hepsin was accompanied by downregulation of TGFβ and EGFR signaling together with a reduction in EGFR protein levels. We further demonstrate in 3D cultures of patient-derived breast cancer explants that neutralizing antibodies and small-molecule inhibitors of hepsin can be used to mitigate the hepsin-induced TGFβ signaling and reduce EGFR protein levels.The study demonstrates a role for hepsin as a regulator of cell proliferation and tumor growth through TGFβ and EGFR pathways, warranting consideration of hepsin as a potential indirect upstream target for therapeutic inhibition of TGFβ and EGFR pathways in cancer.

2023-10-30 | GSE245265 | GEO

High-dose oncogenic PIK3CA drives constitutive cellular stemness through increased NODAL/TGFb signaling

Project description:Oncogenic PIK3CA mutations activate phosphoinositide 3-kinase (PI3K) and are among the commonest somatic mutations in cancer and mosaic, developmental overgrowth disorders. We recently demonstrated that the ‘hotspot’ variant PIK3CAH1047R exerts striking allele dose-dependent effects on stemness in human induced pluripotent stem cells (iPSCs), and moreover demonstrated multiple oncogenic PIK3CA copies in a substantial subset of human cancers. To identify the molecular mechanism underpinning PIK3CAH1047R allele dose-dependent stemness, we profiled isogenic wild-type, PIK3CAWT/H1047R and PIK3CAH1047R/H1047R iPSCs by high-depth transcriptomics, proteomics and reverse-phase protein arrays (RPPA). PIK3CAH1047R/H1047R iPSCs exhibited altered expression of 5644 genes and 248 proteins, whereas heterozygous hPSCs showed 492 and 54 differentially-expressed genes and proteins, respectively, confirming a nearly deterministic phenotypic effect of homozygosity for PIK3CAH1047R. Pathway and network-based analyses predicted a strong association between self-sustained TGFb/NODAL signaling and the ‘locked’ stemness phenotype induced by homozygosity for PIK3CAH1047R. This stemness gene signature was maintained without exogenous NODAL in PIK3CAH1047R/H1047R iPSCs and was reversed by pharmacological inhibition of TGFb/NODAL signaling but not by PIK3CA-specific inhibition. Analysis of PIK3CA-associated human breast cancers revealed increased expression of the stemness markers NODAL and POU5F1 as a function of disease stage and PIK3CAH1047R allele dosage. Together with emerging realization of the link between NODAL re-expression and aggressive cancer behavior, our data suggest that TGFb/NODAL inhibitors warrant testing in advanced breast tumors with multiple oncogenic PIK3CA copies.

2021-03-03 | PXD014719 | Pride

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