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17beta-estradiol (E2)-regulated gene expression across time in estrogen-dependent and estrogen deprivation-resistant MCF-7-derived breast cancer cell lines.

ABSTRACT: A series of MCF-7 variants were previously developed that are either estrogen-dependent for growth (MCF-7:WS8 cells), or resistant to estrogen deprivation and refractory (MCF-7:2A) or sensitive (MCF-7:5C) to E2-induced apoptosis. To identify genes associated with E2-induced apoptosis, estrogen deprivation-resistant/apoptotic-sensitive 5C cells were compared to both estrogen-dependent MCF-7:WS8 and estrogen deprivation/apoptotic-refractory MCF-7:2A cells Each cell line was treated with 10-9 M E2 or vehicle control over a 96 h time course consisting of 7 time points (2, 6, 12, 24, 48, 72 and 96 h) using 6 biological replicates per condition. cRNA probes from individual E2-treated samples were competitively hybridized against time-matched pooled control probes using 2-color Agilent 4x44k human oligonucleotide microarrays.

ORGANISM(S): Homo sapiens

SUBMITTER: Michael Slifker 

PROVIDER: E-GEOD-29917 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Estrogen induces apoptosis in estrogen deprivation-resistant breast cancer through stress responses as identified by global gene expression across time.

Ariazi Eric A EA   Cunliffe Heather E HE   Lewis-Wambi Joan S JS   Slifker Michael J MJ   Willis Amanda L AL   Ramos Pilar P   Tapia Coya C   Kim Helen R HR   Yerrum Smitha S   Sharma Catherine G N CG   Nicolas Emmanuelle E   Balagurunathan Yoganand Y   Ross Eric A EA   Jordan V Craig VC  

Proceedings of the National Academy of Sciences of the United States of America 20111019 47

In laboratory studies, acquired resistance to long-term antihormonal therapy in breast cancer evolves through two phases over 5 y. Phase I develops within 1 y, and tumor growth occurs with either 17β-estradiol (E(2)) or tamoxifen. Phase II resistance develops after 5 y of therapy, and tamoxifen still stimulates growth; however, E(2) paradoxically induces apoptosis. This finding is the basis for the clinical use of estrogen to treat advanced antihormone-resistant breast cancer. We interrogated E(  ...[more]

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