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Expression data from genetically modified HMLE human mammary epithelial cells

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

SUBMITTER: Piyush Gupta

PROVIDER: E-GEOD-24202 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Core epithelial-to-mesenchymal transition interactome gene-expression signature is associated with claudin-low and metaplastic breast cancer subtypes.

Taube Joseph H JH Herschkowitz Jason I JI Komurov Kakajan K Zhou Alicia Y AY Gupta Supriya S Yang Jing J Hartwell Kimberly K Onder Tamer T TT Gupta Piyush B PB Evans Kurt W KW Hollier Brett G BG Ram Prahlad T PT Lander Eric S ES Rosen Jeffrey M JM Weinberg Robert A RA Mani Sendurai A SA

Proceedings of the National Academy of Sciences of the United States of America 20100816 35

The epithelial-to-mesenchymal transition (EMT) produces cancer cells that are invasive, migratory, and exhibit stem cell characteristics, hallmarks of cells that have the potential to generate metastases. Inducers of the EMT include several transcription factors (TFs), such as Goosecoid, Snail, and Twist, as well as the secreted TGF-beta1. Each of these factors is capable, on its own, of inducing an EMT in the human mammary epithelial (HMLE) cell line. However, the interactions between these reg ...[more]

PMID: 20713713

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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.

2010-09-20 | GSE24202 | GEO

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

Project description: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).

2021-03-24 | E-MTAB-9365 | 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

Twist expression in HMLE and breast cancer T47D cells

2013-12-12 | GSE53222 | GEO

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 for HMLE-based EMT models

Project description:Expression data for HMLE-based EMT models

| PRJNA751572 | ENA

Expression data from menadione, PERK inhibitor, or control-treated HMLE-shGFP and HMLE-Twist human mammary epithelial cells

Project description:Malignant carcinomas that recur following therapy are typically de-differentiated and multi-drug resistant (MDR). De-differentiated cancer cells acquire MDR by upregulating reactive oxygen species (ROS)-scavenging enzymes and drug efflux pumps, but how these genes are upregulated in response to de-differentiation is not known. Here, we examine this question by using global transcriptional profiling to identify ROS-induced genes that are already upregulated in de-differentiated cells, even in the absence of oxidative damage. Using this approach, we found that the Nrf2 transcription factor, which is the master regulator of cellular response to oxidative stress, is pre-activated in de-differentiated cells. In de-differentiated cells, Nrf2 is not activated by oxidation but rather through a non-canonical mechanism involving its phosphorylation by the ER membrane kinase PERK. In contrast, differentiated cells require oxidative damage to activate Nrf2. Constitutive PERK-Nrf2 signaling protects de-differentiated cells from chemotherapy by reducing ROS levels and increasing drug efflux. These findings are validated in therapy-resistant basal breast cancer cell lines and animal models, where inhibition of the PERK-Nrf2 signaling axis reversed the MDR of de-differentiated cancer cells. Additionally, analysis of patient tumor datasets showed that a PERK pathway signature correlates strongly with chemotherapy resistance, tumor grade, and overall survival. Collectively, these results indicate that de-differentiated cells upregulate MDR genes via PERK-Nrf2 signaling, and suggest that targeting this pathway could sensitize drug-resistant cells to chemotherapy. Differentiated human breast epithelial cells (HMLE-shGFP) or de-differentiated cells (HMLE-Twist) were treated in culture with 40uM menadione for 2 hours or 1uM PERK inhibitor for 48 hours and compared to control DMSO-treated cells.

2014-10-01 | E-GEOD-59780 | biostudies-arrayexpress

Expression data of mammary epithelial cells during the epithelial-mesenchymal transition

Project description:The EMT program allows epithelial cells to become endowed with motility, invasiveness and stem cell traits. We investigated difference in signaling networks that are differentially utilized in EMTed and non-EMTed cells, thereby identifying therapeutic targets that are unique to EMT/cancer stem cells. We expressed the EMT transcription factors, Twist, Snail and Slug in HMLE human mammary epithelial cells, and compared their gene expression with parental cells. We identified kinases that are more differentially regulated between the epithelial and mesenchymal cell state.

2013-09-09 | E-GEOD-43495 | biostudies-arrayexpress

Effect of GRHL2 in HMLE+Twist-ER+4-OHT cells

Project description:Grainyhead genes are involved in wound healing and developmental neural tube closure. In light of the high degree of similarity between the epithelial-mesenchymal transitions (EMTs) occurring in wound healing processes and the cancer stem cell-like compartment of tumors, including TGF-β-dependence, we investigated the role of a Grainyhead gene (GRHL2) in oncogenic EMT. Grainyhead was specifically down-regulated in the claudin-low subclass of mammary tumors and in the basal-B subclass of breast cancer cell lines. Functionally, GRHL2 suppressed TGF-β-induced, Twist-induced or spontaneous EMT, enhanced anoikis-sensitivity, and suppressed mammosphere generation in mammary epithelial cells. These effects were mediated, in part, by its suppression of ZEB1 expression, through direct repression of the ZEB1 promoter. GRHL2 also inhibited Smad-mediated transcription, and up-regulated mir200b/c as well as the TGF-β receptor antagonist, BMP2. The expression of GRHL2 in the breast cancer cell line MDA-MB-231 triggered a mesenchymal-to-epithelial transition and sensitized the cells to anoikis. These results indicate that GRHL2 is a suppressor of the oncogenic EMT. 3 biologic replicates for each cell line. Comparison of HMLE+Twist-ER cells expressing GRHL2/pMIG vs. HMLE+Twist-ER cells expressing empty pMIG.

2012-02-25 | E-GEOD-36081 | biostudies-arrayexpress

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