Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Transcription profiling of human estrogen-dependent model of breast cancer created by transformation of normal mammary epithelial cells

ABSTRACT: This study was performed to check that ESR1 and BMI1 are biologically active after lentiviral transduction of primary human mammary epithelial cells (HMECs) with lentiviral vectors expressing ESR1 and BMI1 from the human PGK promoter. ESR1 targets like PGR, PRLR and GREB1, but not TFF1 and XBP1, were induced by estradiol in the ESR1-expressing cells. BMI1 targets like BMI1, NEFL and CCND2 were repressed in the BMI1-expressing cells. BMI1 suppressed genes associated with squamous and neural differentiation in the ESR1 plus BMI1-expressing cells. Experiment Overall Design: Infect with lentiviruses 24 hours after reduction mammmoplasty. Grow cells in human mammosphere medium: Hepes-buffered DMEM/F12 supplemented with 20 ng/ml EGF, 1x B-27 (GIBCO) plus 1 nM 17-β-estradiol or 1 uM fulvestrant (ICI 182,780). Experiment Overall Design: Lentiviral vectors: pSD-82, ESR1; pSD-84, BMI1; pSD-86, gusA.

ORGANISM(S): Homo sapiens

SUBMITTER: Richard Iggo 

PROVIDER: E-GEOD-6548 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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An oestrogen-dependent model of breast cancer created by transformation of normal human mammary epithelial cells.

Duss Stephan S   André Sylvie S   Nicoulaz Anne-Laure AL   Fiche Maryse M   Bonnefoi Hervé H   Brisken Cathrin C   Iggo Richard D RD  

Breast cancer research : BCR 20070101 3

<h4>Introduction</h4>About 70% of breast cancers express oestrogen receptor alpha (ESR1/ERalpha) and are oestrogen-dependent for growth. In contrast with the highly proliferative nature of ERalpha-positive tumour cells, ERalpha-positive cells in normal breast tissue rarely proliferate. Because ERalpha expression is rapidly lost when normal human mammary epithelial cells (HMECs) are grown in vitro, breast cancer models derived from HMECs are ERalpha-negative. Currently only tumour cell lines are  ...[more]

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