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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Ganglioside GD2 identifies Breast Cancer Stem Cells: Targeting GD3 Synthase Inhibits GD2 Expression and Tumor Growth

ABSTRACT: We FACS sorted Ras-transformed human mammary epithelial cells (HMLER cells) into GD2+ and GD2- as well as CD44high/CD24low and CD44low/Cd24highcells and comapred the four different population by array. We FACS sorted Ras-transformed human mammary epithelial cells (HMLER cells) into GD2+ and GD2- as well as CD44high/CD24low and CD44low/Cd24highcells and comapred the four different population by array.

ORGANISM(S): Homo sapiens

SUBMITTER: Kurt Evans

PROVIDER: E-GEOD-36643 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Ganglioside GD2 identifies Breast Cancer Stem Cells: Targeting GD3 Synthase Inhibits GD2 Expression and Tumor Growth

Project description:We FACS sorted Ras-transformed human mammary epithelial cells (HMLER cells) into GD2+ and GD2- as well as CD44high/CD24low and CD44low/Cd24highcells and comapred the four different population by array.

2012-04-13 | GSE36643 | GEO

Transcription profiling of human breast tumor epithelia cell types HMLER and BPLER compared to immortalized parent cells of origin - HME and BPE

Project description:The gene expression of two different tumorigenic human breast epithelial cell types (HMLER and BPLER) is compared with their immortalized parental cell-of-origin (HME and BPE). Experiment Overall Design: Two different normal primary human mammary epithelial cell populations (BPECs and HMECs) were isolated based on their differing in vitro growth requirements. These cells were immortalized by hTERT giving rise to BPE and HME cells. These hTERT immortalized cells (BPE and HME) were transformed by SV40-early region (LT+st) and H-Ras giving rise to transformed tumorigenic derivatives BPLER and HMLER. Biological replicates (4 - 6 samples) for each of 4 cell types were analyzed (untransformed hTERT immortalized cell populations (BPE&HME), and transformed tumorigenic derivatives (BPLER & HMLER).

2008-06-15 | E-GEOD-6885 | biostudies-arrayexpress

Identification of EMT and EMT/Cilium-dependent gene expression signatures + Identification of breast tumors of the claudin-low molecular subtype among triple-negative breast cancers

Project description:The goal of the first gene expression analysis reported here (Samples 1-16) was to establish gene expression signatures associated to activation of an Epithelial-Mesenchymal Transition (EMT) and primary ciliogenesis, in immortalized and non-transformed (HMLE) or transformed (HMLER) human mammary epithelial cells, respectively. The goal of the second gene expression analysis (Samples 17-83) was to determine the molecular subtypes of human breast cancers of a triple-negative breast cancer (TNBC) biobank.

2021-10-05 | GSE160549 | GEO

Differential gene expression in epithelial and mesenchymal populations of HMLER cells

Project description:HMLER cells (Ras-transformed version of HMLE cells) were FACS sorted as two subpopulation using CD24 and ITGB4 antibodies. Cells which are negative for CD24 and ITGB4 were mesenchymal in morphology, while cells which are psotive for CD24 and ITGB4 were epithelial. We performed RNA sequencing and expression of several epithelial and mesenchymal phenotype associated proteins were consistent with their mrphology. In addition to the EMT related genes, these two population expressed some unique set of genes.

2022-01-12 | GSE115058 | GEO

EMT inducers catalyze malignant transformation of mammary epithelial cells and drive tumorigenesis towards claudin-low tumors [human]

Project description:The newly identified claudin-low subtype of cancer is believed to represent the most primitive breast malignancies, having arisen from transformation of an early epithelial precursor with inherent stemness properties and metaplastic features. Challenging this hypothesis, we show both in vitro and in vivo that transcription factors inducing epithelial-mesenchymal transition can drive the development of claudin-low tumors from differentiated mammary epithelial cells, by playing a dual role in cell transformation and dedifferentiation. Human mammary epithelial cells (HMEC) were sequentially immortalized by hTert (HMEC-hTert), transduced with Twist1 or Zeb2 or Zeb1 and then with H-RasG12V. The gene expression profiles of the resulting HMEC-hTert-Twist1+Ras, HMEC-hTert-Zeb1+Ras and HMEC-hTert-Zeb2+Ras cell lines were defined. HMEC-hTert-Twist1+Ras and HMEC-hTert-Zeb2+Ras cell lines were additionally cultured in presence of TGFM-CM-^C? and their gene expression profiles were determined. The parental HMEC-hTert, the luminal MCF7 and the basal B MDMB157cell lines were used as controls.

2012-07-23 | E-GEOD-32727 | biostudies-arrayexpress

Transcription profiling of human mesenchymal stem cells transformed with lentiviral vectors of TERT, E6, SV40 and RAS

Project description:Mesenchymal Stem Cells are transformed by step-wise stable transfection with lentiviral vectors of TERT, E6, E7, SV40, and Ras.

2007-04-01 | E-MEXP-563 | biostudies-arrayexpress

Etv4 and Etv5 binding sites in EpRas mouse mammary gland epithelial cell line [ChIP-seq]

Project description:We searched for roles of Etv4 and Etv5 during EMT through genome-wide analysis of their binding sites in Ras-transformed mammary gland epithelial cells.

2017-04-10 | GSE89618 | GEO

Dynamics of MBD2 deposition across methylated DNA regions during malignant transformation of human mammary epithelial cells (2)

Project description:DNA methylation is thought to induce a transcriptional silencing through the combination of two mechanisms: the repulsion of transcriptional activators that do not recognize their binding sites when methylated, and the recruitment of transcriptional repressors that specifically bind methylated DNA. Methyl CpG Binding Domain proteins MeCP2, MBD1 and MBD2 belong to the latter category. However, the exact contribution of each protein in the DNA methylation dependent transcriptional repression occurring during development and diseases remains elusive. Here we present MBD2 ChIPseq data generated from the endogenous protein in an isogenic cellular model of human mammary oncogenic transformation. In immortalized or transformed cells, MBD2 was found in one fourth of methylated regions and associated with transcriptional silencing. Depletion of MBD2 induces upregulations of genes bound by MBD2 and methylated in their transcriptional start site regions. MBD2 was partially redistributed on methylated DNA during oncogenic transformation, independently of DNA methylation changes. Genes downregulated during this transformation preferentially gained MBD2 binding sites on their promoter. Depletion of MBD2 in transformed cells induced the upregulation of some of these repressed genes, independently of the strategy used for the abrogation of oncosuppressive barriers. Our data confirm that MBD2 is a major interpret of DNA methylation, and show an unreported dynamic in this interpretation during oncogenic transformation. RNAseq of untreated HMEC-hTERT cells, siCtrl, siMBD2 or DAC treated HMLER cells, siCtrl or siMBD2 treated HME-ZEB1-RAS and HME-shP53-RAS cells, in duplicates.

2015-06-17 | E-GEOD-63234 | biostudies-arrayexpress

RNA-sequencing of EpH4 and EpRas cells treated with Etv4 and Etv5 siRNAs and/or TGF-beta.

Project description:We performed RNA-seq analysis in mouse mammary gland epithelial EpH4 cell line and its Ras-transformed derivative (EpRas) to analyze the mechanisms of transcriptional regulation during TGF-beta-induced EMT.

2017-04-10 | GSE69363 | GEO

Gene expression profiles of p53 depleted human mammary epithelial cells with their Ras-infected epithelial and mesenchymal derivatives

Project description:The epithelial-mesenchymal transition (EMT) is an embryonic transdiffrentiation program which consists of the conversion of polarized epithelial cells into a motile mesenchymal phenotype. EMT is aberrantly reactivated during tumor progression, promoting metastatic dissemination. Herein, we demonstrate that EMT permissive conditions also favor tumor initiation by minimizing the number of events required for neoplastic transformation. We further demonstrated that even partial commitment of human mammary epithelial cells into an EMT program is sufficient to confer malignant properties, suggesting that the reactivation of embryonic EMT inducers participate to the primary tumor growth long before the initiation of the invasion-metastasis cascade. Human mammary epithelial cells (HMEC) were sequentially depleted in p53 through RNA interference (shp53), transduced with H-RasG12V and immortalized by hTert. Two different Tert/shp53/Ras cell population emerge that display either an epithelial (Epi) or a mesenchymal (Mes) phenotype. Gene expression profiles of the Tert/shp53 control cells and of tert/shp53/Ras/Epi and Tert/shp53/Ras/Mes were analyzed.

2012-01-31 | E-GEOD-26541 | biostudies-arrayexpress

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