Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Effect of estradiol (E2) exposure and KMT2B knockdown on gene expression in MCF-7 cells

ABSTRACT: MCF-7 is an estrogen receptor-positive breast cancer cell line. This experiment is designed to study (1) the effect of estradiol (E2) exposure and (2) lysine methyltransferase 2B (KMT2B) knockdown in MCF-7 cells. Cells were grown for 72 hours prior to treatment with vehicle or 10 nM E2 for 4 and 24 hours. Additionally, to assess the effect of KMT2B knockdown, MCF-7 cells were transfected with KMT2B targeting siRNA or scrambled control siRNA in the absence or presence of E2. RNA were isolated using Trizol and hybridized to Affymetrix GeneChip Human Genome U133 Plus 2.0 array.

INSTRUMENT(S): GeneChip Scanner 3000

ORGANISM(S): Homo sapiens

SUBMITTER: Chia-Hsin Su

PROVIDER: E-MTAB-4923 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Expression data for knockdown of H2ac in E2-treated MCF-7 cell lines

Project description:Estrogens(E2) are important steroid hormones that regulate differentiation, proliferation, and apoptosis in hormone-dependent breast cancer.In order to detect the E2-dependent transcription program associated with the observed cell cycle response, we analyzed the effect of H2ac knockdown on MCF-7 gene expression using microarray. Interestingly, we noticed that 51% of the E2-upregulated genes are down-regulated by depletion of H2ac. The data also show that H2ac regulated E2-dependent genes through E2-induction signaling pathway. MCF-7 cell line was transfected with scrambled or H2ac siRNA in the absence or persence of E2.

2013-07-24 | E-GEOD-39786 | biostudies-arrayexpress

Global survey of miRNA microarray of MCF-7 cells with or without estrogen (E2) treatment

Project description:To examine the effect of E2 treatment for the miRNA expression in human MCF-7 cells, MCF-7 cells were treated with or without E2 (100 nM) for 4 hr or 24 hr. Four group experiments; E2 (100 nM) treatment for 4 hr (MCF-7 E2 4h_1, MCF-7 E2 4h_2), vehicle (ethanol) treatment for 4 hr as Mock control (MCF-7 Mock1, MCF-7 Mock2), E2 (100 nM) treatment for 24 hr (MCF-7 E2 24h_1, MCF-7 E2 24h_2, MCF-7 E2 24h_3), vehicle treatment for 24 hr as Mock control (MCF-7 Mock_3, MCF-7 Mock_4, MCF-7 Mock_5).

2010-05-15 | E-GEOD-16737 | biostudies-arrayexpress

Expression data for knockdown of H2ac in E2-treated MCF-7 cell lines

2013-07-24 | GSE39786 | GEO

Transcriptome analysis of gene expression in MCF-7 cell upon circFAT1(e2) depletion

Project description:In previous study, we found circFAT1(e2) was highly expressed in breast cancer tissues and cell lines. And this factor is also a crucial role in breast cancer genesis and development. So in this study, we knocked down circFAT1(e2) in MCF-7 cells. The viability and metastasis was significantly inhibited with circFAT1(e2) depletion. In order to explore the potential down-stream gene of circFAT1(e2) in breast cancer cells. We extracted the total RNA from circFAT1(e2) knockdown MCF-7 cells and negative control group by using TriZol reagent. Then, toal RNA was subjected to transcriptome sequencing to determine the potential down-stream targets of circFAT1(e2). We expect to reveal the underlied mechanism of the regulatory effect on breast cancer of circFAT1(e2).

2022-12-31 | GSE157343 | GEO

17beta-estradiol (E2)-regulated gene expression across time in estrogen-dependent and estrogen deprivation-resistant MCF-7-derived breast cancer cell lines.

2011-11-21 | GSE29917 | GEO

Global survey of miRNA microarray of MCF-7 cells with or without estrogen (E2) treatment

Project description:To examine the effect of E2 treatment for the miRNA expression in human MCF-7 cells, MCF-7 cells were treated with or without E2 (100 nM) for 4 hr or 24 hr.

2009-07-22 | GSE16737 | GEO

17beta-estradiol (E2)-regulated gene expression across time in estrogen-dependent and estrogen deprivation-resistant MCF-7-derived breast cancer cell lines.

Project description:A series of MCF-7 variants were previously developed that are either estrogen-dependent for growth (MCF-7:WS8 cells), or resistant to estrogen deprivation and refractory (MCF-7:2A) or sensitive (MCF-7:5C) to E2-induced apoptosis. To identify genes associated with E2-induced apoptosis, estrogen deprivation-resistant/apoptotic-sensitive 5C cells were compared to both estrogen-dependent MCF-7:WS8 and estrogen deprivation/apoptotic-refractory MCF-7:2A cells Each cell line was treated with 10-9 M E2 or vehicle control over a 96 h time course consisting of 7 time points (2, 6, 12, 24, 48, 72 and 96 h) using 6 biological replicates per condition. cRNA probes from individual E2-treated samples were competitively hybridized against time-matched pooled control probes using 2-color Agilent 4x44k human oligonucleotide microarrays.

2011-11-21 | E-GEOD-29917 | biostudies-arrayexpress

DHT-AR, E2-AR and R5020-AR target gene profiles in LNCaP

Project description:We previously encountered regulatory processes where dihydrotestosterone (DHT) exerted its inhibitory effect on parathyroid hormone-related protein (PTHrP) gene repression through the estrogen receptor (ER)M-NM-1, but not the androgen receptor (AR) in breast cancer MCF-7 cells. Here, we investigated whether such an aberrant ligand-nuclear receptor (NR) interaction is present in prostate cancer LNCaP cells. First, we confirmed that LNCaP cells expressed a functional AR and at negligible levels of ERM-NM-1, and progesterone receptors. Both suppression of PTHrP and activation of the PSA genes were observed after treatment of E2, DHT and R5020. Consistent with the previous notion that the AR in LNCaP cells lost the ligand specificity due to a mutation AR (Thr-Ala877), our study using siRNA targeting each NR revealed that the AR, but not the other NRs, monopolized the role as the mediator of shared hormone-dependent regulation. These results were invariably associated with nuclear translocation of this mutant AR. Microarray of the genes regulated by either DHT, E2 or R5020 downstream of the AR (Thr-Ala877) revealed that more than half genes overlapped in LNCaP cells. Noticeably, AR (wild-type, wt) and AR (Thr-Ala877) were equally responsible for the E2-AR interactions. Fluorescent microscopic experiments demonstrated that both EGFP-AR (wt) and EGFP-AR (Thr-Ala877) were exclusively localized within the nucleus after E2 or DHT treatment. Further, a promoter assay revealed that breast cancer MCF-7 and Rv22 cells also exhibited such an aberrant E2-AR (wt) signaling. We postulate entangled interactions between the AR (wt) and E2 in a certain hormone-sensitive cancer cells. Total RNAs from the LNCaP cells transfected with control siRNA (siCT) or siRNA for AR (siAR) transfected LNCaP cells before 24 hr followed by exposed to 10-7M of DHT, E2 or R5020 exposure for another 24 h, respectively, were used.

2014-06-19 | E-GEOD-58615 | biostudies-arrayexpress

Effect of estradiol, zearalenone and apigenin on ER-positive breast cancer cells MCF-7

Project description:To understand the molecular effect of E2 and the dietary compound zearalenone and apigenin on MCF-7 proliferation. Results provide insight into the pathway involved by these dietary compounds on MCF-7 proliferation.

2020-07-07 | GSE119552 | GEO

Transcription profiling of uteri from gonadectomized C57BL/6 mice injected with 17-Estradiol (E2) to identify genes modulated by a physiological dose of E2 in uterus.

Project description:17Ã-Estradiol (E2) is well known to be associated with uterine cancer, endometriosis, and leiomyomas. Although insulin-like growth factor I (IGF-I) has been identified as a mediator of the uterotrophic effect of E2 in several studies, this mechanism is still not well understood. In the present study, identification of the genes modulated by a physiological dose of E2, in the uterus, has been done in ovariectomized mice using Affymetrix microarrays. The E2-induced genomic profile shows that multiple genes belonging to the IGF-I pathway are affected after exposure to E2. Two phases of regulation could be identified. First, from 0 to 6 h, the expression of genes involved in the cell cycle, growth factors, protein tyrosine phosphatases, and MAPK phosphatases is quickly upregulated by E2, while IGF-I receptor and several genes of the MAPK and phosphatidylinositol 3-kinase pathways are downregulated. Later, i.e., from 6 to 24 h, transporters and peptidases/proteases are stimulated, whereas defense-related genes are differentially regulated by E2. Finally, cytoarchitectural genes are modulated later. The present data show that a physiological dose of E2 induces, within 24 h, a series of transcriptional events that promote the uterotrophic effect. Among these, the E2-mediated activation of the IGF-I pathway seems to play a pivotal role in the uterotrophic effect. Furthermore, the protein tyrosine phosphatases and MAPK phosphatases are likely to modulate the estrogenic uterotrophic action by targeting, at different steps, the IGF-I pathway. Experiment Overall Design: Ten 10-11 weeks old C57Bl/6 mice were gonadectomized under isoflurane-induced anesthesia and sacrified seven days after GDX. Mice were injected s.c with E2 (0.05ug/mice) or vehicle, at 0.5, 1, 3, 6, 12 or 24 h before sacrifice. Uteri was removed and pooled before total RNA extraction. Samples was hybridized to U74Av2 Genechips (Affymetrix).

2007-11-14 | E-GEOD-6219 | 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