Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

43 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RNA-seq of two human mammary epithelial cell lines (HMLE and HMLE-Twist-ER) treated with 4-hydroxytamoxifen vs control

ABSTRACT: Immortalized non-cancerous human mammary epithelial cells (HMLE) were transfected to express the murine fusion protein Twist1-estrogen receptor(point mutation G525R) (HTER). Twist1-mediated gene expression is activated by stimulation with 4-hydroxytamoxifen for several days and induces an epithelial-mesenchymal transition (EMT) in HTER cells. In breast cancer, EMT equips cancer cells for metastasis and therapy resistance. As control, HTER cells were treated with vehicle (methanol). As additional controls, HMLE cells were stimulated with 4-hydroxytamoxifen or methanol, respectively. Prior to RNA sequencing, EMT-undergoing HTER cells were sorted by fluorescence-activated cell sorting (FACS) based on E-Cadherin and CD44 surface protein levels into three populations, epithelial (E), hybrid epithelial-mesenchymal (EM), and mesenchymal (M): E-Cadherin_high_CD44_low (E), E-Cadherin_medium_CD44_medium (EM), and E-Cadherin_low_CD44_high (M).

INSTRUMENT(S): Illumina HiSeq 2500

ORGANISM(S): Homo sapiens

SUBMITTER: Charlotte Soneson

PROVIDER: E-MTAB-9365 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

MET after transient Twist activation results in de novo gain of malignant traits

Project description:During Epithelial-Mesenchymal Transition (EMT), apical-basal polarized epithelial cells are converted to front-to-back polarized mesenchymal cells that only form loose cell-cell adhesions. These phenotypic changes are accompanied by acquisition of increased motility and invasiveness. EMT programs are orchestrated by pleiotropic transcription factors (TFs), such as Twist1 and Snail1 and effect morphogenetic steps during embryogenesis, including mesoderm formation and neural crest migration. EMTs have also been implicated in the acquisition of aggressive traits by carcinoma cells, including the ability to complete several steps of the metastatic cascade as well as propagation of the tumor by single cells (clonogenicity), a defining trait of tumor-initiating or cancer stem cells. However, the molecular links between the expression of EMT-TFs, the process of EMT and acquisition of clonogenicity remain obscure. Using inducible Twist1 or Snail1 expressed in CD24-positive mammary epithelial cells, we show that clonal growth in anchorage independence and EMT are induced sequentially and independently: clonogenic potential is induced prior to EMT and requires transient TF-activity. By contrast, EMT depends on continuous TF-activation over a longer period. In 3D-collagen assays, continuous Twist1 activity suppresses colony formation, whereas transient activation induces highly invasive growth independently of EMT. In conclusion, our results demonstrate that transient Twist1 activation suffices to drive tumor progression of CD24-positive breast epithelial cells, assessed by invasive as well as anchorage-independent clonal growth, whereas chronic Twist1 exposure can suppress these traits of aggressive tumor cells. We performed gene expression microarray analysis on CD24high and CD24negative populations derived from HMLE-Twist1-ER or HMLE-Snail1-ER cell lines upon various culture conditions

2015-07-02 | E-GEOD-61206 | biostudies-arrayexpress

Expression data for HMLE-based EMT models

Project description:EMT was induced using stable overexpression of 1 of 4 EMT transcription factors (FOXQ1, TWIST1, ZEB2, and SNAI1) in the HMLE cell line. HMLE cells with ectopic LACZ expression were used as control cells.

2021-08-03 | GSE181322 | GEO

Gene expression signature regulated by cell density and Merlin/NF2 knockdown in HMLE cells

Project description:Merlin has been implicated in contact-dependent inhibition of proliferation To define genes regulated by Merlin and study their relationship to cell density-dependent gene expression, microarray experiments were performed after Merlin depletion in HMLE cells at both high and low cell densities. HMLE are non-transformed immortalized human mammary epithelial cells (Elenbaas et al., Genes Dev 15, 2001) HMLE cells were transfected with NF2 or scramble (control) siRNAs. 2 days later medium was changed (dense) or cells seeded in sparse conditions and RNA isolated the day after (3 days after siRNA transfection)

2015-04-01 | E-GEOD-53493 | biostudies-arrayexpress

TWIST1-induced microRNA-424 drives an intermediate epithelial-to-mesenchymal transition that opposes metastasis

Project description:Using a TWIST1-inducible epithelial-to-mesenchymal transition (EMT) model in HMLE cells, miRNA changes were profiled at different time points during an active EMT.

2015-02-26 | GSE58560 | GEO

Twist expression in HMLE and breast cancer T47D cells

2013-12-12 | GSE53222 | GEO

TWIST1-induced microRNA-424 drives an intermediate epithelial-to-mesenchymal transition that opposes metastasis

Project description:Using a TWIST1-inducible epithelial-to-mesenchymal transition (EMT) model in HMLE cells, miRNA changes were profiled at different time points during an active EMT. This experiment includes a total of 12 samples consisting of 2 experimental groups at 2 matching time points (day 4, day 12), each with 3 biological repeats: 3 control empty vector samples as controls and 3 inducible TWIST1 samples as the experimental condition.

2015-02-26 | E-GEOD-58560 | biostudies-arrayexpress

Network Understanding of SNAIL inhibitor induced perturbations in EMT models

Project description:Two engineered HMLE cell lines representing various degrees of EMT were treated with a drug in development to target and inhibit SNAIL interaction with PTP53, called GN-25 total RNA was isolated and analyzed in an Agilent two-color experiment. Four biological replicates of each condition were directly compared, GN25 treated compared to untreated reference The impact of GN-25 on gene expression was investigated using two engineered HMLE cell lines: one stably overexpressing Kras another stably overexpressing Kras and SNAIL

2013-05-31 | E-GEOD-44397 | biostudies-arrayexpress

Snail and Twist expression in HMLE and MCF10A cells

Project description:Snail and Twist are two EMT inducer, expression of Snail or Twist will induce EMT in HMLE and MCF10A cells. By introducing Snail or Twist in HMLE and MCF10A cells, which lack the expression of these two proteins, will identify the genes are induced during EMT. We used microarray analysis to compare the gene expression profiles between the mammamry epithleial cells and the cells undergone EMT.

2020-01-10 | GSE143349 | GEO

Twist expression in HMLE and breast cancer T47D cells

Project description:Twist is a key EMT inducer, expression of Twist will induce EMT in HMLE and breast tumor T47D cells By expressing Twist in HMLE and T47D cells, which lack the expression of Twist, will identify the genes regulated by Twist Expressing Twist in HMLE and T47D cells, stable clones were selected and treated with BET inhibitor JQ1 and RNA were prepared for microarray analysis

2013-12-12 | E-GEOD-53222 | biostudies-arrayexpress

Expression data from genetically modified HMLE human mammary epithelial cells

Project description:Microarrays were used to determine relative global gene expression changes upon introduction of EMT-inducing or control vectors. Experimentally immortalized HMLE breast epithelial cells were retrovirally transduced in culture with vectors encoding EMT-inducing genes or control vectors. There were three biologic replicates for each genetic perturbation condition. After treatment, the cells were selected and expanded, after which total RNA was isolated and subjected to microarray analysis.

2010-09-20 | E-GEOD-24202 | 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