Prostate cancer cell line with slienceing of PDEF or control (GFP) gene using siRNA.
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE6576 | GEO | 2007/12/20
SECONDARY ACCESSION(S): PRJNA98757
REPOSITORIES: GEO
Similar Datasets
Project description:Identifying PDEF regulated genes may shed light on the mechanism by which PDEF may induce breast cancer progression. To that purpose, we have used the MCF-7 human breast tumor cell line model to identify PDEF induced genes. Briefly, PDEF expression was down regulated by shRNA in MCF-7 cells and RNA probes from PDEF-down regulated and control MCF-7 cells were used to screen the Affymetrics HG-U133A Gene Chips. This analysis found 62 genes that were induced 2-fold or higher by PDEF. Further analysis of 3 of these genes namely S100A7, CEACAM6 and B7-H4 in primary breast tumors showed CEACAM6 as a frequently elevated and co-exressed gene with PDEF in these tumors. We previously reported a role for PDEF (prostate derived Ets transcription factor) in breast tumor progression and its association with poor clinical outcome in ER+ breast cancer. To gain further insights into PDEF action in breast cancer, we down regulated PDEF expression by shRNA in MCF-7 human breast tumor cell line, and screened the HG-U133A human gene chips with probes from PDEF down-regulated and control MCF-7 cells. This analysis identified CEACAM6 as one of the genes induced by PDEF. Further analysis of CEACAM6 expression in relation to PDEF in 93 ER+ primary breast tumors showed largely concordant expression of these molecules. To our knowledge, our findings of CEACAM6 as a PDEF induced gene and their elevated co-expression in breast cancer have not been described before.
2012-05-01 | GSE37662 | GEO
Project description:Identifying PDEF regulated genes may shed light on the mechanism by which PDEF may induce breast cancer progression. To that purpose, we have used the MCF-7 human breast tumor cell line model to identify PDEF induced genes. Briefly, PDEF expression was down regulated by shRNA in MCF-7 cells and RNA probes from PDEF-down regulated and control MCF-7 cells were used to screen the Affymetrics HG-U133A Gene Chips. This analysis found 62 genes that were induced 2-fold or higher by PDEF. Further analysis of 3 of these genes namely S100A7, CEACAM6 and B7-H4 in primary breast tumors showed CEACAM6 as a frequently elevated and co-exressed gene with PDEF in these tumors. We previously reported a role for PDEF (prostate derived Ets transcription factor) in breast tumor progression and its association with poor clinical outcome in ER+ breast cancer. To gain further insights into PDEF action in breast cancer, we down regulated PDEF expression by shRNA in MCF-7 human breast tumor cell line, and screened the HG-U133A human gene chips with probes from PDEF down-regulated and control MCF-7 cells. This analysis identified CEACAM6 as one of the genes induced by PDEF. Further analysis of CEACAM6 expression in relation to PDEF in 93 ER+ primary breast tumors showed largely concordant expression of these molecules. To our knowledge, our findings of CEACAM6 as a PDEF induced gene and their elevated co-expression in breast cancer have not been described before. Data from one replicate experiment is included as a representative example of the data obtained. HG-U133A gene chip pairs were screeened with biotinylated RNA probes from PDEF-down regulated MCF-7 cells (experimental) or from control MCF-7 cells.
2012-04-30 | E-GEOD-37662 | biostudies-arrayexpress
Project description:To investigate the role of PDEF in prostate cancer metastasis, we employed microarray analysis of PC3 cells ectopically expressing a pBABE vector control (PC3-SCR) or PDEF-containing vector (PC3-PDEF).
2020-01-24 | GSE108641 | GEO
Project description:Recent studies suggest that PDEF is required for secretory cell differentiation in several epithelial tissues. To investigate PDEF in the mammary gland, we examined the effect of this transcription factor on gene expression using microarray based profiling of MCF-10A cells. These cells are non-transformed mammary epithelial cells that express protein and gene expression programs of basal epithelial cells and undetectable levels of endogenous PDEF. Bioinformatics analysis of the genes induced or repressed by PDEF overexpression in MCF10A cells revealed a striking effect on expression of luminal and myoepithelial cell markers.
2014-03-29 | GSE40986 | GEO
Project description:Microarray gene expression analysis was performed in MCF7 cells transduced with a non-specific shRNA or PDEF-targeting shRNA, and both subjected to hormone depletion for 48 hours. Analyses of differentially expressed genes combined with gene ontology revealed a downregulation of cell cycle related-genes and an upregulation of apoptosis-related genes in PDEF knockdown cells. These target genes constitute potential effectors of the pro-survival role of PDEF.
2014-03-29 | GSE40985 | GEO
Project description:Recent studies suggest that PDEF is required for secretory cell differentiation in several epithelial tissues. To investigate PDEF in the mammary gland, we examined the effect of this transcription factor on gene expression using microarray based profiling of MCF-10A cells. These cells are non-transformed mammary epithelial cells that express protein and gene expression programs of basal epithelial cells and undetectable levels of endogenous PDEF. Bioinformatics analysis of the genes induced or repressed by PDEF overexpression in MCF10A cells revealed a striking effect on expression of luminal and myoepithelial cell markers. Six samples were harvested 26 hours after retroviral infection with either vector control or PDEF. Each condition was performed in triplicate.
2014-03-29 | E-GEOD-40986 | biostudies-arrayexpress
Project description:Microarray gene expression analysis was performed in MCF7 cells transduced with a non-specific shRNA or PDEF-targeting shRNA, and both subjected to hormone depletion for 48 hours. Analyses of differentially expressed genes combined with gene ontology revealed a downregulation of cell cycle related-genes and an upregulation of apoptosis-related genes in PDEF knockdown cells. These target genes constitute potential effectors of the pro-survival role of PDEF. Four samples were harvested after lentiviral infection with either non-specific shRNA control or PDEF-targetting shRNA. All samples were subjected to hormone depletion for 48 hours. Each condition was performed in duplicate
2014-03-29 | E-GEOD-40985 | biostudies-arrayexpress
Project description:This work was conducted to identify shared and specific target genes of different ETS transcription factor rearrangements in prostate cancer. Potential target genes were identified by differential gene expression analysis of primary tumor samples with ETS rearrangements, and validated by ETS silencing in prostate cancer cell lines.
2014-08-12 | GSE42954 | GEO
Project description:This work was conducted to identify shared and specific target genes of different ETS transcription factor rearrangements in prostate cancer. Potential target genes were identified by differential gene expression analysis of primary tumor samples with ETS rearrangements, and validated by ETS silencing in prostate cancer cell lines. The series consists of 50 primary tumor samples from a consecutive series of 200 clinically localized cancers treated with radical prostatectomy at the Portuguese Oncology Institute, Porto, Portugal. The series is enriched in tumors with ETS transcription factor rearrangements
2014-08-12 | E-GEOD-42954 | biostudies-arrayexpress
Project description:ETS gene fusions have been characterized in a majority of prostate cancers, however key molecular alterations in ETS negative cancers are unclear. Here we used an outlier meta-analysis (meta-COPA) to identify SPINK1 outlier-expression exclusively in a subset of ETS rearrangement negative cancers (~10% of total cases). We validated the mutual exclusivity of SPINK1 expression and ETS fusion status, demonstrated that SPINK1 outlier-expression can be detected non-invasively in urine and observed that SPINK1 outlier-expression is an independent predictor of biochemical recurrence after resection. We identified the aggressive 22RV1 cell line as a SPINK1 outlier-expression model, and demonstrate that SPINK1 knockdown in 22RV1 attenuates invasion, suggesting a functional role in ETS rearrangement negative prostate cancers. Keywords: Genetic Modification
2008-06-10 | GSE11132 | GEO