Genes regulated by SMAD3 in HCC cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE132518 | GEO | 2022/06/10
REPOSITORIES: GEO
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Project description:Genes regulated by SMAD3 in HCC cells
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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.
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Project description:The aim of this study is to identify SMAD3 binding targets affected by the TGFb1/SMAD3 signal transduction on a genome-wide scale Formaldehyde cross-linked, sonicated chromatin was prepared from non-stimulated A549 cell line and stimulated with TGFb1. Chromatin immunoprecipated with anti-SMAD3 antibody is labeled with Cy5 and mock IP (with anti-FLAG antibody) is labeled with Cy3 and co-hybridized on Agilent Human Promoter Set arrays. Two biological replicates were performed.
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Project description:The aim of this study is to identify SMAD3 binding targets affected by the TGFb1/SMAD3 signal transduction on a genome-wide scale
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Project description:ChIP seq of endogenous Smad3 and JMJD3 proteins in mouse embryonic neural stem cells treated with TGFbeta during 30 minutes. Neural stem cells were treated with TGFbeta during 30 minutes, and then chromatin immunoprecipitation was carried out with specific JMJD3 or Smad3 antibodies. Positive and negative controls for each immunoprecipitation were checked before sequencing. Input was used to normalized the sequencing results.
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Project description:Atherosclerosis is a persistent inflammatory state accompanied by lipid overload. Vascular fibrosis is one of the primary causes of atherosclerosis development. Although ligustilide (Lig) was shown to exert obvious antiatherogenic effects in previous studies, its precise mechanism has not been comprehensively discussed. In this paper, pharmacologic studies were performed to explore the pharmacodynamic effects of Lig on protecting aorta vascular wall structures and modulating serum inflammatory factors in ApoE-/- mice. Chemical proteomics based on a Lig-derived photoaffinity labelling (Lig-PAL) probe were applied to identify potential therapeutic targets. Mothers against decapentaplegic homologue 3 (SMAD3), which is closely related to the development of vascular fibrosis and atherosclerosis, was identified as a potential target of Lig. Lig suppressed the phosphorylation and nuclear translocation of SMAD3 by blocking the interaction between SMAD3 and transforming growth factor-β (TGF-β) receptor 1, thereby inhibiting the collagen synthesis process, preventing vascular fibrosis and improving atherosclerosis. The quantitative proteomics results from Lig-treated atherosclerotic ApoE-/- mice also indicated that Lig inhibits the expression of collagens I and III, interferes with collagen fibril organization processes and protects the aorta from vascular fibrosis. Hence, developing a novel SMAD3 inhibitor may present another therapeutic option for preventing atherosclerosis.
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Project description:Understanding the molecular mechanisms of pathological vascular remodeling is important for treating cardiovascular diseases and complications. Recent studies have highlighted a role of deubiquitinases in vascular pathophysiology. In this study, we investigated the role of a deubiquitinase, OTUD1, in angiotensin II (Ang II)-induced vascular remodeling. We identified upregulated OTUD1 in the vascular endothelium of Ang II-challenged mice and showed OTUD1 deletion attenuated vascular remodeling, collagen deposition, and EndMT. Conversely, OTUD1 overexpression aggravated these pathological changes both in vivo and in vitro. Mechanistically, SMAD3 was identified as a substrate of OTUD1 using co-immunoprecipitation followed with LC-MS/MS. We found OTUD1 stabilizes SMAD3 and facilitates SMAD3/SMAD4 complex formation and subsequent nuclear translocation through both K48- and K63-linked deubiquitination. OTUD1-mediated SMAD3 activation regulate the transcription of genes involved in vascular EndMT and remodeling in HUVECs. Finally, SMAD3 inhibition reversed OTUD1-promoted vascular remodeling. Our findings demonstrate endothelial OTUD1 promoted Ang II-induced vascular remodeling by deubiquitinating SMAD3. This study identified SMAD3 as a target of OTUD1 and indicates OTUD1 as a potential therapeutic target for the diseases related to vascular remodeling.
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Project description:To find potential microRNA links between Smad3 and E-cadherin, we characterized the microRNA profiles of two gastric cancer cell lines: SNU484-LPCX, which does not express Smad3, and SNU484-Smad3, in which Smad3 is overexpressed. We found that miR-200 families, among other differentially expressed miRNAs, are overexpressed in SNU484-Smad3. Through subsequent studies, including silencing of Smad3 in SNU484-Smad3 and expression profiling of epithelial-mesenchymal markers and ZEB1/2, known repressors of E-cadherin, we found that Smad3 regulates miR-200 families at the transcriptional level, which regulate ZEB 1/2, known transcriptional repressors of E-cadherin, at the post-transcriptional level. This represents an important link between the TGF-beta signaling pathway and post-transcriptional regulation by miRNAs. Examination of small RNA expression in 2 different cell lines (SNU484-LPCX, SNU484-Smad3).
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