Effect of PIAS1 on gene expression
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE44024 | GEO | 2014/02/06
SECONDARY ACCESSION(S): PRJNA188331
REPOSITORIES: GEO
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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.
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2015-05-01 | E-GEOD-62481 | biostudies-arrayexpress
Project description:Mfng, a modulator of Notch signaling, is highly expressed in human claudin-low breast cancer (CLBC). To determine Mfng’s roles in CLBC pathogenesis,we knocked down Mfng in a CLBC cell line MDA-MB231, and found that Mfng knockdown altered Notch activation, decreased tumor sphere formation in vitro, and reduced tumor growth in xenograft model. To identify the potential downstream targets of Mfng during CLBC tumorigenesis, we compared the gene expression profiles between xenografts tumor derived from of MDA-MB231 cells carrying Mfng shRNA and the control vector. Mfng, a modulator of Notch signaling, is highly expressed in human claudin-low breast cancer (CLBC). To determine Mfng’s roles in CLBC pathogenesis,we knocked down Mfng in a CLBC cell line MDA-MB231, and found that Mfng knockdown caused alteration in Notch activation, associated with decreased tumor sphere formation in vitro, as well as reduced tumor growth in xenograft model. We intend to compare gene expression profiles between xenografts of MDA-MB231 cells carrying Mfng shRNA and the control vector. This project seeks to identify potential downstream targets of Mfng in CLBC.
2015-05-01 | GSE62481 | 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.
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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:We report the H3K27ac status in MDA-MB231 breast cancer cells after knockdown of CDK19 and CDK8.
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Project description:To define and compare the interactomes of the RNA binding protein HNRNPC in poorly vs. efficiently metastatic breast adenocarcinoma cells, we carried out immunoprecipitation of endogenous HNRNPC from parental MDA-MB231 cells vs. its highly metastatic isogenic derivate, the MDA-MB231-LM2 cells. We used a non-specific MOUSE IgG IP from each line as control. Each IP was performed in triplicate, and analysed by LC-MS/MS, on a Thermo Q-Exactive-plus instrument.
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Project description:RNA-Seq profiling of triple-negative MDA-MB-231 cell line with know-down of non-canonical WNT signaling receptor Ror1. The MDA-MB231 cells were either transfected with a non-sense control shRNA (shCTL) or with a ROR1 shRNA (shROR1) construct. The objective was to find expression-responsive targets of these perturbations as potential drivers of MDA-MB231 cell invasiveness.
2017-08-17 | GSE96637 | GEO
Project description:Microarray analysis was designed to study the effect of PIAS1 on interferon (IFN) signaling pathway by comparing the gene activation profiles of wild type and Pias1 null cells in response to IFN treatments. Microarray analysis was performed essentially following the manufacturer's instructions (Affymetrix). Briefly, bone marrow-derived macrophages (BMMs) from wile type or Pias1 null littermates were either untreated, or treated with IFN-beta (500 U/ml) or IFN-gamma (10 ng/ml) for 2h or 4h. Total RNA was prepared with RNA-STAT60 (TEL-TEST) and purified with the RNeasy kit (Qiagen). Double stranded complementary DNA was synthesized from 20 ug of total RNA according to Affymetrix methodology, and purified with Phase Lock Gels (Eppendorf). Biotin-labeled RNA was synthesized with the BioArray High Yield RNA Transcript Labeling Kit (Enzo). Samples were cleaned, fragmentated and hybridized to murine genome (MGU74Av2) Genechips (Affymetrix) as instructed. GeneChips were stained with phycoerythrin-streptavidin (Molecular Probes) and scanned with a GeneChip scanner (Affymetrix).
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