Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcriptomic effects of SET7 repression in human breast cancer cells

ABSTRACT: SET7 is a histone methyltransferase suggested to influence gene expression by modifying local chromatin at H3K4me1. RNA-sequencing experiment aimed at identifying the genes regulated by SET7 in MDA-MB-231 cells after SET7 repression. Then comparing the results with those obtained from RNA-seq data after ERRα inactivation (GSE49110) allowed to identify genes regulated by ERRα and SET7.

ORGANISM(S): Homo sapiens

PROVIDER: GSE163017 | GEO | 2021/06/09

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Identification of ERRα target genes in human breast cancer cells

Project description:DNA-binding location of the orphan nuclear receptor ERRα was determined by ChIP-seq in MDA-MB-231 cells

2021-06-09 | GSE163166 | GEO

Gene expression profile in breast cancer cells

Project description:We report the gene expression patterns in MDA-MB-231 (a line selected for low metastatic ability), MDA-MB-231-1833 (its bone-tropic metastatic derivative line), MDA-MB-231p27CK-DD (a phosphomimetic cell line), MDA-MB-231-1833shp27 (p27 knockdown cell line), MDA-MB-231-1833PF1502 (PI3K inhibitor treatment). It shows that the gene expression pattern are regulated in a p27 phosphorylation-dependent manner.

2019-03-19 | GSE112445 | GEO

The miRNA profiling in MDA-MB-231, MDA-MB-231/E1A and knockdown of Dicer in MDA-MB-231/E1A cells

Project description:Dicer, RNase III endonuclease, is an essential enzyme in miRNA biogenesis that regulates target gene expression, and it has been reported that aberrant expressions of Dicer associate with the clinical outcomes of patients in various cancers. To explore the miRNA differencial expression regulated by Dicer in MDA-MB-231/E1A cells, the microarray profiling analysis was employed to conduct differentially expressed miRNAs in stable MDA-MB-231/vector, MDA-MB-231/E1A, and MDA-MB-231/E1A/shDicer cells.

2016-01-16 | GSE76924 | GEO

miRNAs were significantly regulated by myocardin and ERα

Project description:Using microarray, we compared miRNAs expression profiles of MDA-MB-231 cells transfected with myocardin and empty vector (pcDNA3.1) and found that 25 miRNAs were significantly changed in myocardin-transfected groups (17 up-regulated and 9 down-regulated miRNAs). Moreover, we showed that 18 of 25 miRNAs significantly regulated by myocardin were inhibited by ERα in MDA-MB-231 cells. In addition,through a microarray approach, we identify the subset of miRNAs modulated by ERα in MDA-MB-231 cells. Our results determined that ERα may function as tumor-promoter through down-regulating expression of 3 miRNAs (miR-26b, miR-146a and miR-331-3p) in MDA-MB-231 cells.

2014-10-01 | GSE44139 | GEO

Gene-expression profiling of ZNF217-overexpressing MDA-MB-231 cells

Project description:To obtain an overview of the cellular functions regulated by ZNF217 signaling in breast-cancer cell lines, we performed global gene-expression profiling on MDA-MB-231-pcDNA6 and MDA-MB-231-ZNF217 cells

2012-02-06 | GSE35511 | GEO

A novel oncogenic enhancer of estrogen receptor positive breast cancer

Project description:To understand the regulatory landscape of oncogene c-Myc in breast cancer, two epigenetic hallmarks of open chromatin, consisting of H3K4me1 and H3K27ac, were investigated by ChIP-seq in distinct types of human breast cancer cells (estrogen receptor positive MCF-7 and triple-negative MDA-MB-231), respectively. By visualizing the ChIP-seq at c-Myc locus, we noticed that the H3K4me1 and H3K27ac signals were enriched remarkably upstream ~65 kb of c-Myc in MCF-7 cells but not in MDA-MB-231 cells. The results indicated that c-Myc may be regulted by an enhancer located upstream ~65 kb.

2022-10-04 | GSE180080 | GEO

Gene expression data from human breast cancer MDA-MB-231 cells treated with siRNA targeting NONO

Project description:To examine the role of NONO in estrogen-independent breast cancer, MDA-MB-231 cells were treated with siRNA targeting NONO or control siRNA (siControl). Microarray analysis revealed NONO-regulated genes in MDA-MB-231 cells.

2020-01-13 | GSE132742 | GEO

Tang2019 - Pharmacology modelling of AURKB and ZAK interaction in TNBC

Project description:Aurora Kinase B and ZAK interaction model Equivalent of the stochastic model used in "Network pharmacology model predicts combined Aurora B and ZAK inhibition in MDA-MB-231 breast cancer cells" by Tang et. al. 2018. The only difference is cell division and partitioning of the components, which are available in the original model for SGNS2.

2024-09-02 | BIOMD0000000940 | BioModels

The miRNA profiling in MDA-MB-231, MDA-MB-231/E1A and knockdown of Dicer in MDA-MB-231/E1A cells

2016-01-16 | E-GEOD-76924 | biostudies-arrayexpress

Gene expression in human breast cancer cell lines regulated by CXCR6 gene

Project description:This study aimed to further our understanding of the role that CXCR6 plays in breast cancer progression. Microarrays were searched for some genes that had correlated expression with CXCR6 mRNA. According to fold-change screening between restoring expression of CXCR6 and its respective control cells in MDA-MB-231 and MCF-7 cells, both up-regulated and down-regulated genes were shown. The restoring of CXCR6 expression in MDA-MB-231 and MCF-7 cells were respectively noted as MDA-MB-231-CXCR6 and MCF-7-CXCR6 cells and the respective controls were noted as MDA-MB-231-GFP and MCF-7-GFP cells.

2015-06-30 | E-GEOD-60484 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data