Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA143571 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:The majority of breast cancer subtypes express androgen receptor (AR) in addition to estrogen receptor α (ERα). 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 ERα 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
Project description:To study the importance of PIAS1 (protein inhibitor of activated STAT1) for the androgen-regulated transcriptome of VCaP prostate cancer cells, we silenced its expression by RNAi. Transcriptome analyses revealed that a subset of the androgen-regulated genes is significantly influenced, either activated or repressed, by PIAS1 depletion. The depletion also exposed a completely new set of genes to androgen regulation, suggesting that PIAS1 can mask genes from androgen receptor (AR). Pathway analyses of gene expression data suggest involvement of PIAS1 in VCaP cell proliferation. According to genome-wide ChIP-seq analyses, PIAS1 interacts with the AR on chromatin harboring also SUMO2/3, as androgen exposure multiplied the occupancy of PIAS1 in the chromatin, and resulted in nearly complete overlap with AR chromatin binding events. PIAS1 interacted also with pioneer factor FOXA1 in the chromatin. Our results strongly suggest that PIAS1 is a genuine chromatin-bound coregulator of AR which functions in a target gene selective fashion in prostate cancer cells.
2015-01-02 | GSE56086 | GEO
Project description:Analysis of PIAS1 co-regulation in the androgen signaling pathways in prostate cancer cell line. VCaP cells were exposed to control (siSCR) or PIAS1 (siPIAS1) targeted siRNA for 96h. After 16h of 100 nM testosterone (or without) treatment the total RNA was isolated, each treatment included three replicates.
2013-01-01 | E-GEOD-30316 | biostudies-arrayexpress
Project description:To study the effect of PIAS1 on transcriptional regulation, we establishedstable PIAS1 shRNA knockdown cells in breast cancer cell line MDA-MB231. By comparing the expression profiles of control vs PIAS1 knockdown cells, we can identify potential PIAS1 target genes involved in breast tumorigenesis.
2014-02-06 | GSE44024 | GEO
Project description:To study the effect of PIAS1 on transcriptional regulation, we establishedstable PIAS1 shRNA knockdown cells in breast cancer cell line MDA-MB231. By comparing the expression profiles of control vs PIAS1 knockdown cells, we can identify potential PIAS1 target genes involved in breast tumorigenesis. MDA-MB231 Control shRNA and PIAS1 shRNA2 cells were cultured in DMEM plus 10% FBS (DMEM) or SCM for 30 h, and total RNA was used for microarray.
2014-02-06 | E-GEOD-44024 | biostudies-arrayexpress
Project description:The majority of breast cancer subtypes express androgen receptor (AR) in addition to estrogen receptor α (ERα). 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 ERα 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.
2016-07-18 | GSE70162 | GEO
Project description:The majority of breast cancer subtypes express androgen receptor (AR) in addition to estrogen receptor a (ERa). 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 ERa 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.
2016-07-18 | GSE70161 | GEO
Project description:Genome wide analysis of androgen-regulated transcripts
| PRJNA275745 | ENA
Project description:Genome wide analysis of androgen-regulated miRNAs
| PRJNA275744 | ENA
Project description:Heat shock induces rapid modification of proteins with SUMO2/3. This study concentrated in charaterizing how these changes are reflected on SUMOylation of chromatin bound proteins, trancsription, and chromatin binding of SUMO ligase PIAS1. Comparison of chromatin SUMO2/3 modification pattern in non-stressed and heat shocked K562 and VCaP cells. All samples were done as biological replicates. In K562 cells, SUMO2/3 ChIP-seq was done in non-stressed (37C) and heat shocked (30min at 43C) cells. The effect of heat shock factor 1 (HSF1) to chromatin SUMOylation in HS was studied in HSF1 silenced (shHSF1) K562 cells (non-stressed vs. heat shocked) using scramble shRNA transfected cells as control (shSCR). SUMO2/3, SUMO ligase PIAS1,and RNA polymerase II binding in HS (30 min at 43C) and recovery from HS (1h at 37C after HS) was studied using ChIP-seq. Effect of PIAS1 for chromatin SUMOylation was studied in PIAS1 silenced (siRNA for PIAS1, siPIAS1) cells (non-stressed or heat shocked) using non-targeting siRNA transfected cells as a control (siNON). Effect of SUMOylation to chromatin binding of RNA polymerase II was studied in UBE2I silenced (siRNA for UBE2I) and control (non-targeting siRNA transfected, siNON) VCaP cells (non-stressed or heat shocked). Effect of transtription inhibition for chromatin SUMOylation was studied in TRP (triptolide; 1 micromolar, 3h) and DRB (5,6-Dichlorobenzimidazole 1-beta-D-ribofuranosidase; 100 micromolar, 3h) treated VCaP cells. GRO-seq was used to determine HS-induced changes in nascent transcription in K562 cells.
2015-07-02 | E-GEOD-66448 | biostudies-arrayexpress