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Genome-wide analyses of GATA6 occupancy and functions provide insights into its oncogenic mechanisms in human gastric cancer (microarray)

ABSTRACT: To identifiy core GATA6 functions and transcriptional targets in human gastric cancer, including additional subservient transcriptional regulators via integrative analysis of GATA6 transcription factor occupancy, gene dependency, and tumor synexpression. This study used Affymetrix U133A 2.0 gene chips with 2 control and 2 treated replicates for 2 cell types.

ORGANISM(S): Homo sapiens

SUBMITTER: Oliver Hofmann

PROVIDER: E-GEOD-43196 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Genome-wide analyses of GATA6 occupancy and functions provide insights into its oncogenic mechanisms in human gastric cancer (microarray)

Project description:To identifiy core GATA6 functions and transcriptional targets in human gastric cancer, including additional subservient transcriptional regulators via integrative analysis of GATA6 transcription factor occupancy, gene dependency, and tumor synexpression.

2013-12-02 | GSE43196 | GEO

Genome-wide analyses of GATA6 occupancy and functions provide insights into its oncogenic mechanisms in human gastric cancer [ChIP-Seq]

2013-12-02 | GSE51936 | GEO

Genome-wide analyses of GATA6 occupancy and functions provide insights into its oncogenic mechanisms in human gastric cancer [ChIP-Seq]

2013-12-02 | E-GEOD-51936 | biostudies-arrayexpress

Gene expression signature of Gata6 positive epidermal cells.

Project description:To characterize gene expression in Gata6 positive epidermal cells we analyzed a Gata6 reporter mouse in which the endogenous Gata6 promoter drives expression of mTomato. We performed flow cytometry followed by transcriptome analysis. We compared four subpopulations of telogen epidermal cells: Gata6+/Itga6+ cells, Gata6+/itga6- cells, CD34+/Itga6+ cells (which are Gata6-) and all remaining Itga6+ cells (Gata6-/CD34-). The RNA was isolated from age and sex matched mice. We compared four subpopulations of telogen epidermal cells: Gata6+/Itga6+ cells, Gata6+/itga6- cells, CD34+/Itga6+ cells (which are Gata6-) and all remaining Itga6+ cells (Gata6-/CD34-). The RNA was isolated from age and sex matched mice. Three biological replicates for each cell population were analyzed

2017-05-16 | E-GEOD-62606 | biostudies-arrayexpress

Parsing the roles of transcription factors Gata4 and Gata6 in adult cardiac hypertrophic responses

Project description:Cardiac hypertrophy is regulated by the zinc finger-containing DNA binding factors Gata4 and Gata6, both of which are required to mount a productive growth response of the adult heart. To determine if Gata4 and Gata6 are redundant or have non-overlapping roles, we performed cardiomyocyte-specific conditional gene deletions for Gata4 and Gata6 in conjunction with reciprocal replacement with a transgene encoding either Gata4 or Gata6, during the pressure overload response. We determined that Gata4 and Gata6 play a redundant and dosage-sensitive role in programming the hypertrophic growth response itself following pressure overload stimulation. However, non-redundant functions were identified as functional decompensation induced by either Gata4 or Gata6 deletion was not rescued by the reciprocal transgene, and only Gata4 heart-specific deletion produced a reduction in capillary density after pressure overload. Gene expression profiling from hearts of these gene-deleted mice showed both overlapping and unique transcriptional codes, with Gata4 exhibiting the strongest impact. These results indicate that Gata4 and Gata6 play a dosage-dependent and semi-redundant role in programming cardiac hypertrophy, but that each has a unique role in maintaining cardiac homeostasis and adaptation to injury that cannot be compensated by the other. Microarray-bassed gene expression profiling identified overlapping, distinct, and quantitatively/differentially regulated classes of Gata4 or Gata6 regulated genes. To determine if Gata4 and Gata6 are redundant or have non-overlapping roles in programming cardiac hypertrophic responses and adaptation to stress or injury, we performed cardiomyocyte-specific conditional gene deletions for Gata4 and Gata6 in conjunction with reciprocal replacement with a transgene encoding either Gata4 or Gata6, during the pressure overload response.

2014-01-01 | E-GEOD-52317 | biostudies-arrayexpress

Identification of GATA6 target genes in LS174T colorectal cancer cells using gene expression arrays

Project description:Aberrant activation of WNT signaling and loss of BMP signals represent the two main alterations leading to the initiation of colorectal cancer (CRC). Here we screen for genes required for maintaining the tumor stem cell phenotype and identify the zinc-finger transcription factor GATA6 as key regulator of the WNT and BMP pathways in CRC. GATA6 directly drives the expression of LGR5 in adenoma stem cells while it restricts BMP signaling to differentiated tumor cells. Genetic deletion of Gata6 in mouse colon adenomas increases the levels of BMP factors, which signal to block self-renewal of tumor stem cells. In human tumors, GATA6 competes with beta-catenin/TCF4 for binding to a distal regulatory region of the BMP4 locus that has been previously linked to increased susceptibility to develop CRC. Hence, GATA6 creates a permissive environment for tumor stem cell expansion by controlling the major signaling pathways that influence CRC initiation. Total RNA was collected from biological replicates of LS174T colorectal cancer cells transduced with either short hairpin against GATA6 (shGATA6) or non-silencing control (NS) grown in DMEM supplemented with 10% FBS in the presence of doxycycline (dox: 1 Âµg mL-1; Sigma Aldrich) or vehicle (70% ethanol) for a period of 72h. Short hairpins were designed and cloned into doxycycline inducible pTRIPZ lentiviral vector (Open Biosystems). Additionally a 4-hydoxy tamoxifen inducible system was used to inducibly block beta-catenin/TCF activity for a period of 36h. Briefly, the ERT2 domain from the pCMV-CRE-ERT2 (Feil et al., 1996) was amplified by PCR and cloned into a modified FUGW lentiviral vector backbone (Lois et al., 2002). NTCF was then amplified byPCR from the pCDNA3.1-NTCF-NLS (van de Wetering et al., 2002) and cloned in frame upstream of the ERT2 from the FUW-CMV-ERT2 (ET) to create the FUW-CMV-NTCF-ERT2 (NET). Total RNA was extracted using the TRIzolÂ® Plus RNA Purification Kit (Life Technologies).

2014-05-20 | E-GEOD-56895 | biostudies-arrayexpress

Genome-wide map of GATA6 DNA binding in human CRC cells

Project description:We describe the genome-wide DNA-binding of GATA6 in a human CRC cell line (LS174T). GATA6 is found to bind the promoter of genes involved in the maintenance of intestinal stem cells, including genes of the Wnt and TGFbeta/BMP pathways. With this we describe a novel GATA6-dependent mechanism of stem cell maintenance in colorectal tumors. Examination of GATA6 binding and H3K4me1, H3K4me3 and H3K27ac levels in a human CRC cell line by Chromatin immunoprecipitation followed by deep sequencing.

2014-05-20 | E-GEOD-49320 | biostudies-arrayexpress

The transcription factor GATA6 allows self-renewal of colon adenoma stem cells by repressing BMP gene expression.

2014-06-19 | E-GEOD-49479 | biostudies-arrayexpress

ATAC-seq of Het1A cells with overexpression of HNF4A or GATA6

Project description:To determine the ability of HNF4A and GATA6 to drive open chromatin formation, either HNF4A or GATA6 were overexpressed in normal oesophageal Het1A cells and ATAC-seq was performed.

2019-02-04 | E-MTAB-6931 | biostudies-arrayexpress

Genome-wide map of Gata6 DNA binding in mouse pancreas

Project description:We have previously described in mouse models that pancreas-specific deletion of Gata6 results in pancreas alterations by rendering pancreatic acinar cells in a non-fully differentiation state, and furthermore it accelerates tumor initiation and progression in a pro-tumorigenic context (KrasG12V expression). We aim to determine the sites where Gata6 binds at the genome-wide level in the pancreas to unveil why its loss leads to altered pancreatic function and enhanced tumor formation when coexpressed with KrasG12V. Gata6 ChIP-Seq in the mouse pancreas

2015-02-03 | E-GEOD-57090 | biostudies-arrayexpress

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