Dataset Information


Gene expression profiles of MCF-7-derived models of endocrine-resistant breast cancer

ABSTRACT: MCF-7:5C and MCF-7:2A are two in vitro models of Estrogen Receptor alpha positive (ER+) estrogen deprivation-resistant breast cancer. Both cell lines grow robustly in the absence of estrogen [PMID:1301400, PMID:7780972]. MCF-7:PF is an in vitro model of antihormone resistant breast cancer that exhibits the characteristics of acquired tamoxifen resistance [PMID:24183378] The goal of this study was to compare basal levels of gene expression during exponential phase of growth in MCF-7-derived models of endocrine resistance, relative to their isogenic parental cells Overall design: All cell lines were cultured in their respective replete medium. During exponential phase of growth, cells were harvested and total RNA prepared. To compare basal levels of gene expression in MCF-7-derivative cell lines, Cy3-labeled cRNA probes were prepared from each individual isolate harvested from MCF-7:5C, MCF-7:2A, MCF-7:PF and MCF-7:WS8 (including biological replicates where indicated) and co-hybridized with Cy5-labeled cRNA reference probe prepared from untreated MCF-7 parental cells, to Agilent 4x44K dual colour oligonucleotide microarrays.

INSTRUMENT(S): Agilent-014850 Whole Human Genome Microarray 4x44K G4112F (Feature Number version)

SUBMITTER: Heather E. Cunliffe 

PROVIDER: GSE60079 | GEO | 2014-11-30



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Integration of Downstream Signals of Insulin-like Growth Factor-1 Receptor by Endoplasmic Reticulum Stress for Estrogen-Induced Growth or Apoptosis in Breast Cancer Cells.

Fan Ping P   Cunliffe Heather E HE   Maximov Philipp Y PY   Agboke Fadeke A FA   McDaniel Russell E RE   Zou Xiaojun X   Ramos Pilar P   Russell Megan L ML   Jordan V Craig VC  

Molecular cancer research : MCR 20150626 10

Estrogen (E2) exerts a dual function on E2-deprived breast cancer cells, with both initial proliferation and subsequent induction of stress responses to cause apoptosis. However, the mechanism by which E2 integrally regulates cell growth or apoptosis-associated pathways remains to be elucidated. Here, E2 deprivation results in many alterations in stress-responsive pathways. For instance, E2-deprived breast cancer cells had higher basal levels of stress-activated protein kinase, c-Jun N-terminal  ...[more]

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