E-GEOD-60123
Ontology highlight
ABSTRACT:
PROVIDER: E-GEOD-60123 | ExpressionAtlas | 2015-08-25
REPOSITORIES: ExpressionAtlas
Similar Datasets
Project description:Rho-GTPases are small GTP-binding proteins that contribute to the epithelial-to-mesenchymal transition by regulating several cellular processes including organization of the actin cytoskeleton, cell motility, transcription, and cell proliferation. Overexpression of RhoC-GTPases (RhoC) in breast cancer has been implicated in poor disease prognosis due to increased cancer cells invasion, migration, and motility, which warranted its consideration as a therapeutic target for inhibiting breast cancer metastasis. Using silencing RNA (siRNA) molecules to knockdown RhoC expression is a promising approach to inhibit breast cancer metastases.
2015-02-11 | ST000282 | MetabolomicsWorkbench
Project description:Examination of gene expression in response to ING2 knockdown by siRNA in human breast cancer cells
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Project description:To serach gene expression change under knockdown of LRRC26, Leucin Rich Repeat Containing 26 in human triple negative breast cancer cells HCC70, we performed genome-wide DNA microarray analysis and compared the expression levels of control-siRNA treated cells and LRRC26-siRNA treates cells at 48 to 72 h after siRNA transfection
2017-11-30 | GSE90582 | GEO
Project description:The SLC22A18 gene, which encodes an orphan transporter, is located at the 11p15.5 imprinted region, an important tumor-suppressor gene region. However, the role of SLC22A18 in tumor suppression remains unclear. Here, we investigated the involvement of SLC22A18 in cell growth, invasion and drug resistance of MCF7 human breast cancer cell line. Western blot analysis indicated that SLC22A18 is predominantly expressed at intracellular organelle membranes. Quantitative proteomics showed that knockdown of SLC22A18 significantly altered the expression of 578 (31.0%) out of 1867 proteins identified, including proteins related to malignancy and poor prognosis of breast cancer.
2019-06-01 | PXD010183 | JPOST Repository
Project description:We performed RNA-seq to observe the gene expression changes in cells following siRNA-mediated knockdown of DDX3X and DDX54 RNA helicases in human breast cancer MCF7 cells. Two siRNAs were used to target each RNA helicase and scramble siRNA-treated MCF7 cells were used as controls.
2018-11-21 | E-MTAB-6235 | biostudies-arrayexpress
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:In previous studies, we identified a distantly related rhomboid homologue gene known as RHBDD2 (Rhomboid domain containing 2) to be markedly overexpressed in the advanced stages of the breast and colorectal cancer diseases. In order to identify RHBDD2 modulated pathways, we analyzed two breast cancer cell lines (MCF7 and T47D) from control and RHBDD2-siRNA transient gene silencing followed by gene expression profiling analysis using the whole genome Toray 3D-GeneTM Human Oligo Chip. Statistical analysis of the Toray's 3D gene expression profiling data identified 566 commonly differentially expressed genes in association to the RHBDD2 knockdown in both breast cancer cell lines. Among the statistically significant over-represented biological process, we found the apoptosis, cell cycle and response to DNA damage process related genes. In addition, categories of genes found in the ubiquitin-proteasome and oxidative phosphorylation were also highly enriched related genes in the commonly deregulated gene list. We further used a lentivirus-based system (shRNA-pLKO.1) for stable silencing of RHBDD2 mRNA in the T47D breast cancer cell line. Using a staurosporine-induced apoptosis model, we demonstrate that RHBDD2 abrogation resulted in an apoptosis-resistant phenotype of T47D breast cancer cell line. These data are in line with a recent study, suggesting that RHBDD2 expression could be up-modulated in response to 5FU-induced apoptosis in colorectal cancer cells. Taken together, these data suggest that RHBDD2 could be involved in the modulation of the programmed cell death in cancer cells. In order to analyze differential gene expression profiling of RHBDD2 silencing and control cells, total RNA was isolated from replicate experiments from two breast cancer cell lines (MCF7 and T47D) derived from the negative control-siRNA and the RHBDD2-siRNA treatments in duplicate experiments.
2013-04-10 | E-GEOD-43015 | biostudies-arrayexpress
Project description:We profiled transcriptomes in human breast cancer cell line T47D when the expression of HOTAIR was knockdown by the siRNA specific to an HOTAIR isoform HOTAIR-N (NR_047517).
2018-09-06 | GSE119511 | GEO
Project description:Estrogen receptor M-NM-1 (ERM-NM-1) is a nuclear receptor that is the driving transcription factor expressed in the majority of breast cancers. Recent studies have demonstrated that the liver receptor homolog-1 (LRH-1), another nuclear receptor, is ERM-NM-1-regulated in breast cancer cells. Further, LRH-1 stimulates proliferation and promotes motility and invasion of breast cancer cells. To determine the mechanisms of LRH-1 action in breast cancer cells, we carried out gene expression microarray analysis following siRNA-mediated LRH-1 knockdown. Interestingly, gene ontology (GO) category enrichment analysis of the genes differentially regulated in the presence or absence of LRH-1 identified estrogen responsive genes as the most highly enriched GO categories. To further define LRH-1 target genes, we performed chromatin immunoprecipitation coupled to massively parallel sequencing (ChIP-seq) to identify genomic targets of LRH-1. Remarkably, ChIP-seq showed LRH-1 binding at many ERM-NM-1 binding sites. Analysis of select binding sites confirmed regulation of ERM-NM-1-regulated genes by LRH-1 through binding to estrogen response elements, as exemplified by the TFF1/pS2 gene. Finally, LRH-1 over-expression stimulated ERM-NM-1 recruitment, whilst LRH-1 knockdown reduced ERM-NM-1 recruitment to ERM-NM-1 binding sites. Taken together, our findings establish a key role for LRH-1 in the regulation of ERM-NM-1 target genes in breast cancer cells and identify a mechanism in which co-operative binding of LRH-1 and ERM-NM-1 at estrogen response elements controls the expression of estrogen-responsive genes. MCF-7 cells were transfected with LRH-1 siRNA #2, #3, or with a non-targeting siRNA (siControl) for 72 hours. Following assessment of RNA integrity, four biological replicates for each siRNA treatment were used for microarray analysis.
2013-09-01 | E-GEOD-47803 | biostudies-arrayexpress
Project description:Study of loss of ZEB2 in breast cancer cells in vitro and in vivo: gene expression and phenotypic switch to more benign behavior of the cancer cells. Morphological, functional and gene microarray analysis following ZEB2 knockdown in MDAMB231 cells reveals gain of epithelial differentiation, reduction of migration, invasion and metastatic capability. The measurement of ZEB2 transcriptional activity in tumor cells efficiently predicts the probability of breast cancer patient survival. Global gene expression profiles were measured using Affymetrix U133 plus2 microarrays in MDAMB231 cells (control and ZEB2 shRNA and siRNA knockdown cells on plastic)
2016-03-15 | E-GEOD-27966 | biostudies-arrayexpress