Homo sapiens
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ABSTRACT:
PROVIDER: PRJNA284106 | ENA |
REPOSITORIES: ENA
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Project description:Using a siRNA screen we identified the histone demethylase enzyme KDM3A as a potential positive regulator of ER signalling in breast cancer. To interrogate the full extent of KDM3A regulation on ER signalling we assessed basal and estrogen (E2)- stimulated global gene expression changes in KDM3A-depleted MCF-7 cells by microarray analysis using the Illumina Human HT12 Version 4 BeadChip array. We identified ER regulated genes affected by KDM3A knockdown and determined that KDM3A is required for ER recruitment to estrogen response elements in the promotors of ER regulated genes. We also identified that KDM3A regulates expression of a number of genes involved in proliferation and that knockdown of KDM3A inhibits ER positive breast cancer cell growth.
2015-05-16 | GSE68918 | GEO
Project description:Using a siRNA screen we identified the histone demethylase enzyme KDM3A as a potential positive regulator of ER signalling in breast cancer. To interrogate the full extent of KDM3A regulation on ER signalling we assessed basal and estrogen (E2)- stimulated global gene expression changes in KDM3A-depleted MCF-7 cells by microarray analysis using the Illumina Human HT12 Version 4 BeadChip array. We identified ER regulated genes affected by KDM3A knockdown and determined that KDM3A is required for ER recruitment to estrogen response elements in the promotors of ER regulated genes. We also identified that KDM3A regulates expression of a number of genes involved in proliferation and that knockdown of KDM3A inhibits ER positive breast cancer cell growth. MCF-7 cells were transfected with either a non-silencing scrambled control siRNA (siSCR) or a KDM3A targeting siRNA (siKDM3A-B) using Lipfectamine RNAiMAX (Invitrogen) to a final concentration of 25 nM in steroid depleted conditions. Cells were grown for 48 hours prior to treatment with vehicle or 10 nM E2 for 4 hours before RNA extraction using TRIzol (Ambion, Life Technologies) and hybridization of triplicate samples to an Illumine HT-12 v4 BeadChip array. One sample failed due to low amounts of cRNA and was therefore not included in the analysis (siKDM3A + E2 Replicate 3). The array for replicates 1 and 2 was performed in August 2013 (Array 1) and replicate 3 in August 2014 (Array 2). When processing the data Array 2 was normalized to Array 1.
2015-05-16 | E-GEOD-68918 | biostudies-arrayexpress
Project description:To elucidate the KDM4B regulated transcriptomes in ER-positive breast cancer cells we assessed global gene expression changes in KDM4B-depleted MCF-7 cells by microarray analysis using the Illumina Human HT12 Version 4 BeadChip array. Differentially expressed genes were compared with KDM3A and FOXA1 regulated transcriptomes. We identified 229 genes co-regulated by all three enzymes and that co-regulated genes were involved in cell cycle processes. We identified that 53% and 48% of KDM4B-regulated genes were also regulated by KDM3A and FOXA1, with co-regulatory gene signatures being involved with estrogen response signatures and cell proliferation. We also identified that depletion of KDM3A and KDM4B together inhibits ER-target gene expression and ER-positive breast cancer cell growth more than depletion of either gene on its own.
2019-08-06 | GSE135427 | GEO
Project description:To interrogate the extent of overlap between KDM3A and FOXA1 regulated transcriptomes in ER-positive breast cancer cells we assessed global gene expression changes in KDM3A-depleted and FOXA1-depleted MCF-7 cells by microarray analysis using the Illumina Human HT12 Version 4 BeadChip array. We identified that 43% of the KDM3A regulated transcriptome was also regulated by FOXA1 and that 43% of the FOXA1 regulated transcriptome was also regulated by KDM3A. Genes co-regulated by KDM3A and FOXA1 were involved in ER-signalling and the cell growth. We also identified that depletion of KDM3A was required for the deposition of FOXA1 on chromatin.
2019-08-07 | GSE124270 | GEO
Project description:Identification of overlap between KDM3A and FOXA1 regulated transcriptome in the ER positive breast cancer cell line MCF-7
| PRJNA511446 | ENA
Project description:Identification of the KDM4B regulated transcriptome in the ER positive breast cancer cell line MCF-7
| PRJNA558818 | ENA
Project description:Breast cancer invasive growth, metastasis and therapeutic resistance affects the clinical ourcome. We explored the epigenetic mechanisms that control these process in breast cancer cell line, MDA-MB-231 by knocking down a lysine specific demethylase KDM3A We used microarrays to detail the global programme of gene expression underlying cellularisation and identified distinct classes of up-regulated genes during this process. Human breast cancer cell line MDA-MB-231 was infected with scramble or KDM3A shRNA. After selection, the cells were used for microarray analysis.
2016-06-29 | E-GEOD-83818 | biostudies-arrayexpress
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: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:Estrogen receptor-α (ERα) is an important driver of breast cancer and is the target for hormonal therapies, anti-estrogens and drugs that limit estrogen biosynthesis (aromatase inhibitors). Mutations in the ESR1 gene identified in metastatic breast cancer provide a potential mechanism for acquired resistance to hormone therapies. We have used CRISPR-Cas9 mediated genome editing in the MCF-7 breast cancer cell line, generating MCF-7-Y537S. MCF-7-Y537S cells encode a wild-type (tyrosine 537) and a mutant (serine 537) allele. Growth of the line is estrogen-independent and expression of ERα target genes is elevated in the absence of estrogen. ER ChIP-seq was carried out to map global ERα binding sites in the presence and absence of estrogen. RNA-seq following estrogen treatment was used for gene expression analysis. We show that expression of ER target genes and ER recruitment to ER binding regions is similar in MCF-7 and MCF-7-Y537S cells, except that ER recruitment to DNA and expression of ER target genes is frequently elevated in the absence of estrogen.
2016-10-25 | GSE78285 | GEO