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Coordinated Chromatin Remodeling induced by Demethylation requires SRCAP mediated H2A.Z exchange

ABSTRACT: This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

ORGANISM(S): Homo sapiens

SUBMITTER: Houtan Noushmehr

PROVIDER: E-GEOD-26685 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Gene reactivation by 5-aza-2'-deoxycytidine-induced demethylation requires SRCAP-mediated H2A.Z insertion to establish nucleosome depleted regions.

Yang Xiaojing X Noushmehr Houtan H Han Han H Andreu-Vieyra Claudia C Liang Gangning G Jones Peter A PA

PLoS genetics 20120329 3

5-Aza-2'-deoxycytidine, approved by the FDA for the treatment of myelodysplastic syndrome (MDS), is incorporated into the DNA of dividing cells where it specifically inhibits DNA methylation by forming covalent complexes with the DNA methyltransferases (DNMTs). In an effort to study the correlations between DNA methylation, nucleosome remodeling, and gene reactivation, we investigate the integrated epigenetic events that worked coordinately to reprogram the methylated and closed promoters back t ...[more]

PMID: 22479200

Similar Datasets

Coordinated Chromatin Remodeling induced by Demethylation requires SRCAP mediated H2A.Z exchange [Methylation]

Project description:Genome wide DNA methylation profiling of RKO cells with combination treatments of non-target siRNA or SRCAP siRNA and PBS or 1uM 5-Aza-CdR treatment. The Illumina Infinium 27k Human DNA methylation Beadchip v1.2 was used to obtain DNA methylation profiles across 27,578 CpGs in treated RKO cells. Samples included cells under 4 different treatments. The sample treated with non target siRNA and PBS serves as control sample. Bisulphite converted DNA from the 4 samples were hybridised to the Illumina Infinium 27k Human Methylation Beadchip v1.2

2013-01-01 | E-GEOD-26433 | biostudies-arrayexpress

Coordinated Chromatin Remodeling induced by Demethylation requires SRCAP mediated H2A.Z exchange [expression]

Project description:Genome wide gene expression profiling of RKO cells with combination treatments of non-target siRNA or SRCAP siRNA and PBS or 1uM 5-Aza-CdR treatment. The sample treated with non target siRNA and PBS serves as control sample. Total RNA obtained from isolated RKO cells.

2013-01-01 | E-GEOD-26684 | biostudies-arrayexpress

Genetic deletion of osteopontin in TRAMP mice enhances the growth of aggressive prostate cancer with feature of human neuroendocrine tumors

Project description:Osteopontin (OPN) is a secreted glycoprotein, belonging to the non-structural extracellular matrix (ECM), and its over expression in human prostate cancer cells has been associated with disease progression, androgen independence and metastases. Nevertheless the pathophysiology of OPN in prostate tumorigenesis has never been studied. We crossed TRansgenic Adenocarcinoma of the Mouse Prostate (TRAMP) mice with OPN deficient (OPN-/-) mice and followed tumor onset and progression in these double mutants. Ultrasound examination detected the early onset of a spherical homogeneous tumor in about 60% of OPN-/- TRAMP mice that seldom occurs in parental TRAMP mice. Histology and immunohistochemistry characterized these tumors for being Tag positive but negative for AR, highly proliferative and endowed of neuroendocrine (NE) features. Gene expression profiling showed up-regulation of genes involved in tumor progression, cell cycle and neuronal differentiation in OPN-deficient versus -sufficient TRAMP tumors. Down-regulated genes included key genes of TGFï?¢ pathway, and a role for TGFï?¢ in NE differentiation of prostate cancer was also confirmed at the protein level. Furthermore, NE genes and particularly those characterizing early prostatic lesions of OPN-deficient mice were found to correlate with those of human NE tumours. These data underscore a novel role of OPN at early stages of prostate cancer growth, protecting against the development of aggressive NE tumors. Total RNA obtained from prostate tumors from 18 and 30 weeks old TRAMP mice, compared to RNA extracted from prostate tumors and prostate tissue from Osteopontin-deleted TRAMP mice

2016-01-20 | E-GEOD-69903 | biostudies-arrayexpress

Robust Differentiation of Islet Progenitors into Functional Insulin-secreting Cells by Suppression of Key Transcription Regulators

Project description:Gene profiling revealed that differentiation was accompanied by suppression of a range of transcription regulator genes typical of islet progenitor cells. In order to understand molecular mechanisms of differentiation, transcriptome-wide gene expression analysis was performed on purified islet progenitors at days 0, 1 and 4 of differentiation together with adult islets as a control. In order to understand molecular mechanisms of differentiation, transcriptome-wide gene expression analysis was performed on purified islet progenitors at days 0, 1 and 4 of differentiation together with adult islets as a control.

2013-11-01 | E-GEOD-51944 | biostudies-arrayexpress

SUMOylation modulates the transcriptional activity of androgen receptor in a target gene and pathway selective manner.

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2014-07-03 | E-GEOD-54202 | biostudies-arrayexpress

hsa-miR-199a-3p is an oncosuppressor microRNA in papillary thyroid carcinoma

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2014-06-30 | E-GEOD-49415 | biostudies-arrayexpress

Risk of T1D progression in islet autoantibody positive children can be further stratified using expression patterns of multiple genes implicated in peripheral blood lymphocyte activation and function

Project description:To identify genes with expression levels that are associated with T1D progression from AbP (islet autoantibody positive), global gene expression changes were analyzed in AbP subjects with different T1D progression rate. Total RNA were obtained from peripheral blood mononuclear cells (PBMC) of total 36 AbP subjects with different T1D progression rate. Microarray was carried out to analyze gene expression and Kaplan-Meier survival analysis and log-rank test were used to compare differences in diabetes-free survival between groups classified based on single gene expression.

2014-04-10 | E-GEOD-51058 | biostudies-arrayexpress

Wnt signalling sustains an EpiSCs subpopulation similar to primitive streak with increased mesendodermal potency

Project description:During gastrulation, epiblast cells are pluripotent and their fate is thought to be constrained principally by their position. Cell fate is progressively restricted by localised signalling cues from areas including the primitive streak (PS). However, it is unknown whether this restriction accompanies, at the single cell level, a reduction in potency. Investigation of these early transition events in vitro is possible via the use of Epiblast Stem Cells (EpiSCs), self-renewing pluripotent cell lines equivalent to the postimplantation epiblast. Strikingly, EpiSCs express various early lineage-specific markers in self-renewing conditions. However, it is unknown whether cells that express these markers are pluripotent, spontaneously differentiated, or biased towards specific lineages. Here we show that EpiSC are inherently heterogeneous and contain two major and mutually exclusive subpopulations with PS and neural characteristics respectively. Using differentiation assays and embryo grafting we demonstrate that PS-like EpiSCs are biased towards mesoderm and endoderm differentiation but they still retain their pluripotent character. The acquisition of a PS character by undifferentiated EpiSC is mediated by paracrine Wnt signalling. Elevation of Wnt activity promotes further restriction into PS-associated cell fates which occurs via the generation of distinct clonal mesendodermal and neuromesodermal precursors. Collectively, our data suggest that primed pluripotency encompasses a range of reversible lineage-biased states reflecting the birth of pioneer lineage precursors from a pool of uncommitted EpiSCs similar to the earliest cell fate restriction events taking place in the gastrula-stage epiblast. Total RNA obtained (3 biological replicates) from flow sorted dsRed2+, dsRed2-, and +CHIRON treated for 48h cells was isolated and labelled/amplified using the IlluminaM-BM-. TotalPrepM-bM-^DM-" RNA Amplification Kit (Life Technologies)

2014-03-04 | E-GEOD-48476 | biostudies-arrayexpress

Genome-wide analysis of androgen receptor (AR) SUMOylation effects on gene expression (HEK293).

Project description:Androgen receptor (AR) plays an important regulatory role during prostate cancer development. ARM-bM-^@M-^Ys transcriptional activity is regulated by androgenic ligands, but also by post-translational modifications. To study the role of the AR SUMOylation in genuine chromatin environment, we compared androgen-regulated gene expression and AR chromatin occupancy in PC-3 prostate cancer and HEK293 cell lines stably expressing wild-type (wt) or SUMOylation site-mutated AR (AR-K386R,K520R). Our genome-wide gene expression analyses reveal that the SUMOylation modulates the AR function in a target gene and pathway selective manner. The transcripts that are differentially regulated by androgen and SUMOylation are linked to cellular movement, cell death, cellular proliferation, cellular development and cell cycle. In line with these data, SUMOylation mutant AR cells proliferate faster and are more sensitive to apoptosis. Moreover, ChIP-seq analyses show that the SUMOylation modulates the chromatin occupancy of AR on many loci in a fashion that parallels with their differential androgen-regulated expression. De novo motif analyses show that other transcription factor-binding motifs are differentially enriched at the wtAR- and the AR-K386R,K520R-preferred genomic binding positions. Taken together, our data indicate that SUMOylation does not simply repress the AR activity, but it regulates ARM-bM-^@M-^Ys interaction with the chromatin and the receptorM-bM-^@M-^Ys target gene selection. Isogenic HEK293 cells stably expressing wild-type AR (wtAR) or SUMOylation-defective AR (AR-K2R) were treated 24 h with 10 nM R1881 or vehicle (EtOH). All conditions were performed in triplicate. The effect on gene expression was assessed by microarray.

2014-07-03 | E-GEOD-54137 | biostudies-arrayexpress

Genome-wide analysis of PIAS1 on AR gene expression in MDA-MB453

Project description:The majority of breast cancer subtypes express androgen receptor (AR) in addition to estrogen receptor Î± (ERÎ±). Depending on the breast cancer subtype androgen signaling has either stimulatory or inhibitory roles in breast cancer cell growth. We have mapped AR cistrome in ERÎ± negative human molecular apocrine breast cancer MDA-MB453 cells and analyzed it in relation to the androgen-regulated transcriptome in the same cells. We have also examined the effect of silencing of the coregulator SUMO ligase PIAS1 on the androgen-regulated transcriptome and AR cistrome in MDA-MB453 cells. Our results show that the MDA-MB453 cells share with VCaP prostate cancer cells a core AR cistrome and target gene signature linked to cancer cell growth and that PIAS1 acts as an AR target gene-selective coregulator in MDA-MB453 cells. MDA-MB453 cells were transfected with control siRNA (siNON) or PIAS1 siRNA (siPIAS1) for 72 h and treated 16 h with 10 nM R1881 or vehicle (ethanol). Total RNA was isolated and biological triplicate samples were analyzed by microarray.

2016-07-18 | E-GEOD-70162 | biostudies-arrayexpress

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