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Chip-chip from HepG2 cells and HepG2 cells with slug overexpression

ABSTRACT: The transcription factor slug represses genes with E-box and then activates cancer stem cell related pathway: Wnt, Notch and Hedgehog pathway. Chromatin immunoprecipitation (ChIP) of slug by ChIP-on-chip analysis demonstrated that slug indirectly activates cancer stem cell related pathway and thus promotes vasculogenic mimicry formation.

ORGANISM(S): Homo sapiens

PROVIDER: GSE41027 | GEO | 2012/09/21

SECONDARY ACCESSION(S): PRJNA175582

REPOSITORIES: GEO

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Chip-chip from HepG2 cells and HepG2 cells with slug overexpression

Project description:The transcription factor slug represses genes with E-box and then activates cancer stem cell related pathway: Wnt, Notch and Hedgehog pathway. Chromatin immunoprecipitation (ChIP) of slug by ChIP-on-chip analysis demonstrated that slug indirectly activates cancer stem cell related pathway and thus promotes vasculogenic mimicry formation. Comparison of HepG2-control in regular culture, HepG2-slug in regular culture and HepG2-slug on Matrigel.

2012-09-21 | E-GEOD-41027 | biostudies-arrayexpress

Expression analysis of HepG2, HepG2-slug and HepG2-slug on Matrigel

Project description:Investigation of whole genome gene expression level changes in hepatocellular carcinoma cell line hepG2 in regular culture, hepG2-slug in regular culture and hepG2-slug on Matrigel. Whole genome gene expression level changes have been compared in hepatocellular carcinoma cell line hepG2 in regular culture, hepG2-slug in regular culture and hepG2-slug on Matrigel. Roche NimbleGen micro-array analysis was employed to assess global genome expression in HepG2 in regular culture, HepG2-slug in regular culture and HepG2-slug on Matrigel. The results demonstrated that the up-regulated genes and the down-regulated genes increased significantly when HepG2-slug cells with VM forming ablity were cultured on Matrigel and formed VM.

2012-09-21 | E-GEOD-41026 | biostudies-arrayexpress

Expression analysis of HepG2, HepG2-slug and HepG2-slug on Matrigel

2012-09-21 | GSE41026 | GEO

Slug overexpression

Project description:This SuperSeries is composed of the following subset Series: GSE41026: Expression analysis of HepG2, HepG2-slug and HepG2-slug on Matrigel GSE41027: Chip-chip from HepG2 cells and HepG2 cells with slug overexpression Refer to individual Series

2012-09-21 | E-GEOD-41028 | biostudies-arrayexpress

Gene expression of osteosarcama cell line with vasculogenic mimicry phenotype

Project description:Vasculogenic mimicry has been generally accepted as a new form of tumor vascularization and regarded as an unfavorable prognostic factor in multiple aggressive malignancies. We previously reported the presence of vasculogenic mimicry in osteosarcoma patients. The mechanistic basis for osteosarcoma VM remains unclear. We used microarrays to detail the global programme of gene expression between 143B cells and HOS cells exposed to Matrigel which showed greatly different vasculogenic mimicry formation potential and identified distinct classes of vasculogenic mimicry-realted genes during this process.

2018-09-15 | GSE119975 | GEO

Targeting the vulnerability of arachidonic acid metabolism to enhance immunotherapy efficacy in ARID1A-deficient colorectal cancer [ChIP-Seq]

Project description:ARID1A, a core constituent of SWI/SNF complex, is mutated in about 10% of colorectal cancer (CRC). This study demonstrates a synergistic effect of arachidonic acid metabolism inhibitors with immune checkpoint inhibitors (ICIs) by regulating functionality of CD8+ T cells and vasculogenic mimicry (VM) formation in ARID1A-deficient CRC. Mechanistically, ATAC-seq and ChIP-qPCR demonstrated that the lack of ARID1A results in reduced levels of the key enzymes PTGS1 and PTGS2, which control the arachidonic acid pathway. This reduction generated a reliance on the remaining functionality of arachidonic acid pathway in ARID1A-deficient cells.

2024-11-26 | GSE278082 | GEO

Slug-dependent UVR induction of cytokines and chemokines

Project description:Studies of the zinc finger transcription factors Slug and Snail have largely focused on their important role in modulating epithelial-mesenchymal transition during embryonic development and tumor progression. However, these transcription factors also appear to regulate local inflammation. In previous studies, we showed that Slug knockout mice were resistant to sunburn, an acute cutaneous inflammatory response, compared to wild type mice. In the present studies, we used Slug knockout, chimeric Slug knockout/wild type, conditional Slug knockout, and Slug transgenic mice to study the role of Slug in ultraviolet radiation (UVR)-induced cutaneous inflammation. We demonstrated, using immunohistochemistry, in vivo imaging, and neutrophil migration studies, that it was Slug expression in the epidermis rather than in neutrophils that modulated the UVR response. Microarray analysis indicated that this modulation was effected by the production of epidermal cytokines, including CCL3, CCL4, oncostatin, and interleukin-1β, that recruited neutrophils to UVR-exposed skin. The pattern of pro-inflammatory gene regulation by Slug suggested a central role for NF-κB in mediating gene induction. Immunohistochemical analysis of UVR-induced NF-κB activation demonstrated reduced activation in Slug knockout and enhanced activation in Slug transgenic epidermis. Slug thus appears to modulate NF-κB activation in response to UVR.

2016-08-27 | GSE86107 | GEO

The invasion promoter Slug is a critical cell cycle regulator

Project description:Background: The well-characterized function of the transcriptional repressor, Slug, is to promote EMT and tumor invasion/metastasis by down-regulating E-cadherin expression. In this study, we investigated the significance of Slug during the S phase. Method: Slug mRNA expression was isolated from thymidine-arrested CL1-5/AS2neo (control) and CL1-5/AS2neo-Slug-WT stable cells. The Agilent oligonucleotide microarray analysis was performed to identify Slug downstream genes. Results: Overexpression of Slug inhibited lung [3H]-thymidine incorporation and delayed S phase progression. By using Agilent microarray we have identified panel of genes altered by Slug overexpression. Slug can down-regulate target genes about cell cycle networks for DNA replication, DNA replication checkpoint and genomic stability, such as TOP1, ORC4, RFC3, and Rad17. Conclusions: the multifaceted role of Slug in cancer progression by controlling the epithelial-mesenchymal transition and genome stability.

2012-02-09 | GSE35617 | GEO

The invasion promoter Slug is a critical cell cycle regulator

2012-02-09 | E-GEOD-35617 | biostudies-arrayexpress

The transcription Factor Slug represses p16Ink4a and regulates murine muscle stem cell aging

Project description:Sustainable muscle regeneration necessitates proper maintenance of the quiescence-reversible SCs pool. Activation of p16Ink4a-associated senescence pathway during aging breaks muscle homeostasis and causes degenerative muscle disease by irreversibly dampening satellite cell (SC) self-renewal capacity. We performed microarrays analysis to compare the genome-wide gene expression profiles of wild-type and Slug-deficient SCs and identified distinct classes of up-regulated genes upon deletion of Slug gene.

2019-03-20 | GSE128507 | GEO

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