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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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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. Comparison of HepG2-control in regular culture, HepG2-slug in regular culture and HepG2-slug on Matrigel.

ORGANISM(S): Homo sapiens

SUBMITTER: baocun sun

PROVIDER: E-GEOD-41027 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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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

ChIP-DSL H20K promoter array from human gastric cancer cells MKN28 with Sox2 overexpression

Project description:The transcription factor Sox2 inhibits human gastric cancer growth and activates Sox2-related tumor surpressive genes in human gastric cancer cells. Conditional Sox2-overexpression in cells with a low Sox2 level demonstrated that the Sox2-regulated tumor surpressive genes demand on an enhanced Sox2 activity for better expression to work in human gastric cancer. Chromatin immunoprecipitation (ChIP) of Sox2 together with chromatin profiling by ChIP-on-chip analysis demonstrated that Sox2 directly activates the chromatin at promoters or putative enhancers of Sox2 target genes. Transcription factor Sox2 promoter array in MKN28 cells with Sox2 overexpression.

2013-05-22 | E-GEOD-45427 | biostudies-arrayexpress

Chip-chip from HepG2 cells with EZH2, SUZ12 and H3K27me3

Project description:Polycomb group (PcG) proteins including EZH2, SUZ12 and so on, which specifically catalyze trimethylation of histone 3 lysine 27 (H3K27me3), and methylated H3K27 can be recognized by other specific binding proteins to compress chromatin structure, leading to the transcriptional repression of the target genes. To completely understand the epigenetic profile and molecular network of PcG in HCC, we performed ChIP-on-chip screens with EZH2, SUZ12 and H3K27me3 antibodies in HepG2 cells. Comparison of ChIP-on-chip results from EZH2, SUZ12 and H3K27me3.

2013-11-13 | E-GEOD-52300 | biostudies-arrayexpress

Altered expression of microRNAs in bone metastasis compared with human prostate cancer

Project description:The principal problem arising from prostate cancer (PCa) is its propensity to metastasize to bone. MicroRNAs (miRNAs) play a crucial role in many tumor metastases.The importance of miRNAs in bone metastasis of PCa has not been elucidated to date. We investigated whether the expression of certain miRNAs was associated with bone metastasis of PCa. We examined the miRNA expression profiles of 6 primary and 7 bone metastatic PCa samples by miRNA microarray analysis. Total RNA was taken from the specimens, low molecular weight RNA was seperate and labeled , and then hybridized to capitalbio V3.0 biochip representing about 924 microRNA.

2011-01-31 | E-GEOD-26964 | 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

Transcriptional profiling of HCC vs. Normal liver and Pericancer vs. Normal liver.

Project description:Hepatocellular carcinoma (HCC) is one of the most malignant and lethal cancers in the world. Its complex process of molecular pathogenesis indicates that HCC is caused by multiple etiological factors and involves multiple types of genes during its development and progression. In the current study, we performed a microarray analysis on the mRNA transcriptome of HCC (C), peri-cancerous liver (P) and normal liver (N) tissues. After integrating these results with information from the Gene Ontology and KEGG Pathway databases, we analyzed the potential interactions between different genes and constructed an interaction network, and identified the regulator, mediator and effector genes in this interaction network. Three types of tissues: 49 pairs of homogenous human primary hepatocellular carcinoma (Cancer, C) and pericancer liver tissues (Pericancer, P), 10 normal liver tissues (Normal, N). Three-condition experiment, HCC vs. Normal and Pericancer vs. Normal.

2013-03-14 | E-GEOD-45114 | biostudies-arrayexpress

The chromatin modifier CHD8 targets autism risk genes during human neurodevelopmentM-BM-

Project description:Whole-exome sequencing studies have implicated chromatin modifiers and transcriptional regulators in autism spectrum disorder (ASD) through the identification of de novo loss of function mutations in affected individuals. Many of these genes are co-expressed in mid-fetal human cortex, suggesting ASD risk genes converge in regulatory networks that are perturbed in ASD during neurodevelopment. To elucidate such networks we mapped promoters and enhancers bound by the chromodomain helicase CHD8, which is strongly enriched in ASD-associated de novo loss of function mutations, using ChIP-seq in mid-fetal human brain, human neural stem cells (hNSCs), and embryonic mouse cortex. We find that CHD8 targets are strongly enriched for ASD risk genes that converge in ASD-associated co-expression networks in human midfetal cortex. CHD8 knockdown in hNSCs results in significant dysregulation of ASD risk genes targeted by CHD8, as well as additional genes important for neurodevelopment, including members of the Wnt/M-NM-2-catenin signaling pathway. Integration of CHD8 binding data with genetic and gene co-expression data in ASD risk models provides support for additional ASD risk genes. Together, our results suggest that loss of CHD8 function contributes to ASD through regulatory perturbation of other ASD risk genes during human cortical development. Two biological replicates for each ChIP with appropriate Input control Four biological replicates for each condition in knockdown experiments (Ctrl construct, Chd8 target C, and Chd8 target G)

2015-01-21 | E-GEOD-57369 | biostudies-arrayexpress

Analysis of micorRNA expression during the HBV acute and chronic infections

Project description:Recent implication of microRNAs (miRNAs) in the intricate cross-talk between the host and the pathogen in viral infections reveals a new layer of mechanism for host-virus interactions. In the present study, we investigated human miRNAs which may be involved in the acute and chronic HBV infections via microarray profiling. We determined the global miRNA expression profiles elicited in the uninfected control model (HepG2), the acute infection model (HepG2 transfected with a 1.3 full-length HBV genome) and the chronic infection model (HepG2.2.15) using CapitalBio corporation’s mammalian miRNA arrays. Three cellular models were used in this study: the human hepatoblastoma cell line HepG2 as a blank control representing the condition without virus infection; HepG2 transfected with a 1.3 full-length HBV genome as an acute infection model; and HepG2.2.15, a well-established cell line derived from HepG2 transfected with a full-length HBV genome and constitutively expressing HBV, as a chronic infection model.

2010-06-16 | E-GEOD-22378 | biostudies-arrayexpress

Comparative genomics of the srd1 null mutant Candida albicans strain CaLY202.

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2014-06-24 | E-GEOD-48530 | biostudies-arrayexpress

Comparative genomics of a fluconazole-resistant variant Candida albicans strain CaLY188.

Project description:To investigate the diversity of gene contents of Candida albicans strain by array-based comparative genomic hybridization (array CGH; aCGH). A fluconazole-resistant variant Candida albicans strain CaLY188 was selected to carry out the comparative genomics microarray. Two-condition experiment, CaLY188 vs.SN152. Biological replicates: 2 control, 2 transfected, independently grown and harvested. One replicate per array.

2014-06-24 | E-GEOD-48529 | biostudies-arrayexpress

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