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Genome-wide gene expression analysis by TEAD4 knockdown in a gastric cancer cell line SNU216

ABSTRACT: To access oncogenic roles of TEAD4 in gastric cancer, TEAD4-regulated genes were investigated using a SNU216 cell line in which TEAD4 expression was knockdown by shRNA. To compare control to TEAD4 knockdown cell, total RNA was extracted from two cell lines generated by non-silencing shRNA control and TEAD4 knockdown.

ORGANISM(S): Homo sapiens

SUBMITTER: Byungho Lim

PROVIDER: E-GEOD-44383 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Integrative genomics analysis reveals the multilevel dysregulation and oncogenic characteristics of TEAD4 in gastric cancer.

Lim Byungho B Park Jong-Lyul JL Kim Hee-Jin HJ Park Young-Kyu YK Kim Jeong-Hwan JH Sohn Hyun Ahm HA Noh Seung-Moo SM Song Kyu-Sang KS Kim Woo-Ho WH Kim Yong Sung YS Kim Seon-Young SY

Carcinogenesis 20131209 5

Tumorigenesis is a consequence of failures of multistep defense mechanisms against deleterious perturbations that occur at the genomic, epigenomic, transcriptomic and proteomic levels. To uncover previously unrecognized genes that undergo multilevel perturbations in gastric cancer (GC), we integrated epigenomic and transcriptomic approaches using two recently developed tools: MENT and GENT. This integrative analysis revealed that nine Hippo pathway-related genes, including components [FAT, JUB, ...[more]

PMID: 24325916

Similar Datasets

Genome-wide gene expression analysis by TEAD4 knockdown in a gastric cancer cell line SNU216

Project description:To access oncogenic roles of TEAD4 in gastric cancer, TEAD4-regulated genes were investigated using a SNU216 cell line in which TEAD4 expression was knockdown by shRNA.

2014-01-02 | GSE44383 | GEO

Genome-wide binding of TEAD4 in gastric cancer cell lines MKN28 and SNU216

Project description:To access target binding sites of TEAD4 in gastric cancer, TEAD4 binding was investigated using MKN28 and SNU216 cell lines by ChIP-seq. MKN28 and SNU216 cell lines were cross-linked with formaldehyde, fractionated by sonication and immunoprecipitated by TEAD4 antibody. Immunoprecipitated DNA was prepared by generating libraries and sequenced by massive parallel sequencing.

2014-01-02 | E-GEOD-44416 | biostudies-arrayexpress

Genome-wide binding of TEAD4 in gastric cancer cell lines MKN28 and SNU216

Project description:To access target binding sites of TEAD4 in gastric cancer, TEAD4 binding was investigated using MKN28 and SNU216 cell lines by ChIP-seq.

2014-01-02 | GSE44416 | GEO

Identification of TEAD4 target genes in colorectal cancer cells

Project description:We have identified TEAD4 as a key prognosis factor in colorectal cancer. To elucidate the potentail mechanism and function of TEAD4 in colorectal caner, we generated two stable cell lines expressing different shRNA targeting TEAD4 in the mesenchymal-like LoVo cells and the differential genes were detected by microarray. LoVo colorectal cancer cells stably expressing pLKO.1 control shRNA or sh1_shTEAD4 or sh2_shTEAD4

2014-01-01 | E-GEOD-53063 | biostudies-arrayexpress

TEAD4 occupied genes in differentiated C2C12 myoblasts

Project description:The TEAD (1-4) transcription factors comprise the conserved TEA/ATTS DNA binding domain recognising the MCAT element in the promoters of muscle-specific genes. Despite extensive genetic analysis, the function of TEAD factors in muscle differentiation has proved elusive due to redundancy amongst the family members. Expression of the TEA/ATTS DNA binding domain that acts a dominant negative repressor of TEAD factors in C2C12 myoblasts inhibits their differentiation, while selective shRNA knockdown of TEAD4 results in abnormal differentiation characterised by the formation of shortened myotubes. Chromatin immunoprecipitation coupled to array hybridisation (ChIP-chip) shows that TEAD4 occupies 867 promoters including those of myogenic miRNAs. We show that TEAD factors cooperate with MYOD1 to directly induce Myogenin, CDKN1A and Caveolin 3 expression to promote myoblast differentiation and fusion. RNA-seq identifies a novel set of TEAD4 target genes encoding muscle structural and regulatory proteins and those required for the unfolded protein response. In contrast, TEAD4 represses expression of the growth factor CTGF and Cyclin D1 to promote differentiation. Together these results show that TEAD factor activity is essential for C2C12 cell differentiation and define a novel and nonredundant role for TEAD4 in regulating the unfolded protein response. C2C12 cells were infected with retrotiviral vector expressing Flag-HA-Tagged TEAD4 or with empty control vector and selected in the continouos presence of puromycin. Infected cell populations were then differentiated for 5 days in DMEM medium with 2% horse serum and fixed in 0.4% formaldehyde.

2011-08-21 | E-GEOD-29208 | biostudies-arrayexpress

Identification of TEAD4 target genes in colorectal cancer cells

2014-01-01 | GSE53063 | GEO

TEAD4 regulated genes in differentiated C2C12 myoblasts

2011-08-22 | GSE27845 | GEO

TEAD4 occupied genes in differentiated C2C12 myoblasts

2011-08-22 | GSE29208 | GEO

TEAD4

Project description:TEAD4

| PRJNA604980 | ENA

Altered Subcellular Localization of Transcription Factor TEAD4 Regulates First Mammalian Cell Lineage Commitment

Project description:In the preimplantation mouse embryo TEAD4 is critical to establishing the trophectoderm (TE)-specific transcriptional program and segregating TE from the inner cell mass (ICM). However, TEAD4 is expressed both in the TE and the ICM. Thus, differential function of TEAD4 rather than expression itself regulates specification of the first two cell lineages. We used ChIP-seq to define genome-wide TEAD4 target genes and asked how transcription of TEAD4 target genes is specifically maintained in the TE. Our analyses revealed an evolutionarily conserved mechanism, in which lack of nuclear localization of TEAD4 impairs the TE-specific transcriptional program in inner blastomeres, thereby allowing their maturation towards the ICM lineage. Restoration of TEAD4 nuclear localization maintains the TE-specific transcriptional program in the inner blastomeres and prevents segregation of the TE and ICM lineages and blastocyst formation. We propose that altered subcellular localization of TEAD4 in blastomeres dictates first mammalian cell fate specification. ChIPseq profiles of TEAD4, IgG, Input in Mouse trophoblast stem cells using Illumina HiSeq 2000 and Illumina Genome Analyzer IIx

2012-04-18 | E-GEOD-37350 | biostudies-arrayexpress

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