Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

Transcription profiling of human estrogen-responsive breast cancer cell lines treated with 17beta-estradiol for 1 to 32 hours

ABSTRACT: Human estrogen-responsive breast cancer cell lines ZR-75-1 and MCF-7 were treated with 10nM of 17beta-estradiol. Gene expression was analyzed on total RNA extracted before or after 1, 2, 4, 6, 8, 12, 16, 20, 24, 28 and 32 hours hormonal stimulation. For each condition 2 technical replicates were performed, except the reference sample (before stimulation - 0h) which was in respectively in quadruplicate and quintuplicate.

ORGANISM(S): Homo sapiens

SUBMITTER: Alessandro Weisz

PROVIDER: E-TABM-742 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Estrogen receptor alpha controls a gene network in luminal-like breast cancer cells comprising multiple transcription factors and microRNAs.

Cicatiello Luigi L Mutarelli Margherita M Grober Oli M V OM Paris Ornella O Ferraro Lorenzo L Ravo Maria M Tarallo Roberta R Luo Shujun S Schroth Gary P GP Seifert Martin M Zinser Christian C Chiusano Maria Luisa ML Traini Alessandra A De Bortoli Michele M Weisz Alessandro A

The American journal of pathology 20100326 5

Luminal-like breast tumor cells express estrogen receptor alpha (ERalpha), a member of the nuclear receptor family of ligand-activated transcription factors that controls their proliferation, survival, and functional status. To identify the molecular determinants of this hormone-responsive tumor phenotype, a comprehensive genome-wide analysis was performed in estrogen stimulated MCF-7 and ZR-75.1 cells by integrating time-course mRNA expression profiling with global mapping of genomic ERalpha bi ...[more]

PMID: 20348243

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Project description:We are using ACI and BN rats, which differ markedly in their susceptibility to 17beta-Estradiol (E2)-induced mammary cancer, to identify genetic variants and environmental factors that determine mammary cancer susceptibility. The objective of this study was to characterize the cellular and molecular responses to E2 in the mammary glands of ACI and BN rats to identify qualitative and quantitative phenotypes that associate with and/or may confer differences in susceptibility to mammary cancer. Female ACI and BN rats were treated with E2 for 1, 3 or 12 weeks and cell proliferation, apoptosis, differentiation and gene expression were evaluated. The luminal epithelium of ACI rats exhibited a rapid and sustained proliferative response to E2. By contrast, the proliferative response exhibited by the mammary epithelium of BN rats was restrained and transitory. Moreover, the epithelium of BN rats appeared to undergo differentiation in response to E2, as evidenced by production of milk proteins as well as luminal ectasia and associated changes in the extracellular matrix (ECM). Marked differences in expression of genes that encode proteins with well-defined roles in mammary gland development (Pgr, Wnt4, Tnfsf11, Prlr, Stat5a, Areg, Gata3), differentiation and milk production (Lcn2, Spp1), regulation of extracellular environment (Mmp7, Mmp9), and cell-cell or cell-ECM interactions (Cd44, Cd24, Cd52) were observed. We propose that these cellular and molecular phenotypes are heritable and may underlie, at least in part, the differences in mammary cancer susceptibility exhibited by ACI and BN rats. Two groups of 17beta-estradiol treated female rats were compared. Five ACI and five BN rats were treated with 17beta-estradiol for 12 weeks. Total RNA was isolated from the mammary glands of these animals, labeled, and hybridized to Affymetrix Rat Genome 230 2.0 Arrays (Affymetrix Inc.). Significantly differentially expressed genes were found between these groups.

Dataset Information

Transcription profiling of human estrogen-responsive breast cancer cell lines treated with 17beta-estradiol for 1 to 32 hours

Publications

Estrogen receptor alpha controls a gene network in luminal-like breast cancer cells comprising multiple transcription factors and microRNAs.

Similar Datasets

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