E-GEOD-37087
Ontology highlight
ABSTRACT:
PROVIDER: E-GEOD-37087 | ExpressionAtlas | 2015-08-18
REPOSITORIES: ExpressionAtlas
Similar Datasets
Project description:Transcriptional profiling of human MCF-7 breast cancer cells comparing MCF-7 cells treated with control medium (DMEM/F12 + 0,5% BSA) with MCF-7 cells treated with conditioned medium of cancer-associated adipose tissue (CMCAAT) obtained from 2 breast cancer patients. Goal was to determine the effects of CMCAAT treatment on global MCF-7 gene expression.
2015-01-07 | GSE58574 | GEO
Project description:MDA-MB-231 breast cancer cells and MCF-10A breast cells were exposed to 1 mT 50 Hz extremely low-frequency magnetic field (ELF-MF) for 4 hours
2023-02-17 | PXD040120 | JPOST Repository
Project description:Purpose: AURKA plays an important role in breast cancer development. Exploring the gene expression profiles regulated by AURKA will facilitate to understand the mechanism which is responsible for AURKA induced breast cancer development. Results: We found that 350 genes were significantly up-regulated during AURKA overexpression in MCF-10A cells, 346 genes were significantly down-regulated during AURKA overexpression in MCF-10A cells. Conclusions: Our study indicated that 696 differentially expressed genes might contribute to AURKA induced breast cancer development. MCF-10A cells overexpressed AURKA or the empty vector were subjected to RNA extraction. The resulted RNA samples were performed RNA-sequencing analyses of gene expression profiles.
2015-10-28 | E-GEOD-57931 | biostudies-arrayexpress
Project description:Purpose: AURKA plays an important role in breast cancer development. Exploring the gene expression profiles regulated by AURKA will facilitate to understand the mechanism which is responsible for AURKA induced breast cancer development. Results: We found that 350 genes were significantly up-regulated during AURKA overexpression in MCF-10A cells, 346 genes were significantly down-regulated during AURKA overexpression in MCF-10A cells. Conclusions: Our study indicated that 696 differentially expressed genes might contribute to AURKA induced breast cancer development.
2015-10-28 | GSE57931 | GEO
Project description:Previously, we have shown that HIST1H2ac is overexpressed in MCF-7 breast cancer cell line. It acts as a master regulator of estrogen receptor alpha-dependent gene expression in ER+ breast cancer cells. In the present study, we investigate the genome-wide protein DNA-binding events of HIST1H2ac protein in MCF-7 breast cancer cell line by over-expressing hemagglutinin (HA)-tagged HIST1H2ac and compared with MCF-7 cells over-expressing HA. The protein-bound DNA was recovered by immunoprecipitation using anti-HA antibody. The ChIP DNA and input DNA were sequenced with an Illumina HiSeq 2000 sequencer.
2016-05-19 | E-MTAB-3160 | biostudies-arrayexpress
Project description:A significant fraction of breast cancers exhibit de novo or acquired resistance to estrogen deprivation. A kinome-wide siRNA screen identified a role for Insulin Receptor (InsR) in the hormone-independent growth of ER+ breast cancer cells We used gene expression microarrays to identify genes and pathways that are altered by insulin stimulation of ER+ MCF-7 human breast cancer cells. MCF-7 cells were treated with serum-free medium +/- insulin for 4 or 24 hrs prior to RNA harvest for analysis.
2012-04-10 | E-GEOD-28580 | biostudies-arrayexpress
Project description:The study aims to elucidate the effect of histone H2A.ZK102me2 on gene expression in MCF-7 breast cancer cell line. Results provide insight into the role of H2A.ZK102me2 in breast cancer cell.
2016-11-17 | GSE58047 | 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: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:Despite improvements in therapeutic strategies for treating breast cancers, tumor relapse and chemoresistance remain major issues in patient outcomes. Indeed, cancer cells display a metabolic plasticity allowing a quick adaptation to tumoral microenvironment and to cellular stresses induced by chemotherapy. Recently, long non-coding RNA molecules (lncRNAs) have emerged as important regulators of cellular metabolic orientation. In the present study, we addressed the role of the long non-coding RNA molecule (lncRNA) SAMMSON on the metabolic reprogramming and chemoresistance of MCF-7 breast cancer cells resistant to doxorubicin (MCF-7dox). Our results showed an overexpression of SAMMSON in MCF-7dox compared to doxorubicin-sensitive cells (MCF-7). Silencing of SAMMSON expression by siRNA in MCF-7dox cells resulted in a metabolic rewiring with improvement of oxidative metabolism, decreased mitochondrial ROS production, increased mitochondrial replication, transcription and translation and an attenuation of chemoresistance. These results highlight the role of SAMMSON in the metabolic adaptations leading to the development of chemoresistance in breast cancer cells. Thus, targeting SAMMSON expression levels represents a promising therapeutic route to circumvent doxorubicin resistance in breast cancers.
2021-11-10 | GSE188404 | GEO