Genome-wide analysis of the effect of PIAS1 knockdown by siRNA on the androgen regulated gene programs
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE30316 | GEO | 2013/01/01
SECONDARY ACCESSION(S): PRJNA143571
REPOSITORIES: GEO
Similar Datasets
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 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: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: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 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:Crosstalk of androgen signaling induced with dihydrotestosterone (DHT) and proinflammatory signaling induced with tumor necrosis-factor alpha (TNFa) was analyzed in prostate cancer cells (LNCaP) by following chromatin binding of androgen receptor (AR), p65 (activating subunit of nuclear-factor kappa-B [NFkB]), FOXA1 and PIAS1+2 chromatin binding using ChIP-seq and transcriptional changes using GRO-seq.
2016-10-05 | GSE83860 | GEO
Project description:Although the vital role of the androgen receptor (AR) has been well demonstrated in primary prostate cancers, its role in the androgen-insensitive prostate cancers still remains unclear. Here, we used a small hairpin RNA approach to directly assess AR activity in prostate cancer cells. Reduction of AR expression in the two androgen-sensitive prostate cancer cell lines, LNCaP and LAPC4, significantly decreased AR-mediated transcription and cell growth. Intriguingly, in two androgen-insensitive prostate cell lines, LNCaP-C42B4 and CWR22Rv1, knockdown of AR expression showed a more pronounced effect on AR-induced transcription and cell growth than androgen depletion. Using cDNA microarrays, we also compared the transcriptional profiles induced by either androgen depletion or AR knockdown. Although a significant number of transcripts appear to be regulated by both androgen depletion and AR knockdown, we observed a subset of transcripts affected only by androgen depletion but not by AR knockdown, and vice versa. Finally, we demonstrated a direct role for AR in promoting tumor formation and growth in a xenograft model. Taken together, our results elucidate an important role for the AR in androgen-insensitive prostate cancer cells, and suggest that AR can be used as a therapeutic target for androgen-insensitive prostate cancers. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set Computed
2007-08-08 | E-GEOD-7585 | biostudies-arrayexpress
Project description:Although the vital role of the androgen receptor (AR) has been well demonstrated in primary prostate cancers, its role in the androgen-insensitive prostate cancers still remains unclear. Here, we used a small hairpin RNA approach to directly assess AR activity in prostate cancer cells. Reduction of AR expression in the two androgen-sensitive prostate cancer cell lines, LNCaP and LAPC4, significantly decreased AR-mediated transcription and cell growth. Intriguingly, in two androgen-insensitive prostate cell lines, LNCaP-C42B4 and CWR22Rv1, knockdown of AR expression showed a more pronounced effect on AR-induced transcription and cell growth than androgen depletion. Using cDNA microarrays, we also compared the transcriptional profiles induced by either androgen depletion or AR knockdown. Although a significant number of transcripts appear to be regulated by both androgen depletion and AR knockdown, we observed a subset of transcripts affected only by androgen depletion but not by AR knockdown, and vice versa. Finally, we demonstrated a direct role for AR in promoting tumor formation and growth in a xenograft model. Taken together, our results elucidate an important role for the AR in androgen-insensitive prostate cancer cells, and suggest that AR can be used as a therapeutic target for androgen-insensitive prostate cancers. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set
2007-08-09 | GSE7585 | GEO