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Series GSE27473 Query DataSets for GSE27473
Status Public on May 01, 2011
Title Expression data from MCF7 cell line after silencing of Estrogen receptor
Organism Homo sapiens
Experiment type Expression profiling by array
Summary We propose the hypothesis that loss of estrogen receptor function which leads to endocrine resistance in breast cancer, also results in de-differentiation from an epithelial to a mesenchymal phenotype that is responsible for increased aggressiveness and metastatic propensity. siRNA mediated silencing of the estrogen receptor in MCF7 breast cancer cells resulted in estrogen/tamoxifen resistant cells (pII) with altered morphology, increased motility with rearrangement and switch from an actin to a vimentin based cytoskeleton, and ability to invade simulated components of the extracellular matrix. Phenotypic profiling using an Affymetrix Human Genome U133 plus 2.0 GeneChip indicated fold changes ≥ 3 in approximately 2500 identifiable unique sequences, with about 1270 of these being up-regulated in pII cells. Changes were associated with genes whose products are involved in cell motility, loss of cellular adhesion and interaction with the extracellular matrix. Selective analysis of the data also showed a shift from luminal to basal cell markers and increased expression of a wide spectrum of genes normally associated with mesenchymal characteristics, with consequent loss of epithelial specific markers. Over-expression of several peptide growth factors and their receptors are indicative of an increased contribution to the higher proliferative rates of pII cells as well as aiding their potential for metastatic activity. Signalling molecules that have been identified as key transcriptional drivers of epithelial to mesenchymal transition were also found to be elevated in pII cells. We suggest that these data support our hypothesis that induced loss of estrogen receptor in previously antiestrogen sensitive cells is a trigger for the concomitant loss of endocrine dependence and onset of a series of possibly parallel events that changes the cell from an epithelial to a mesenchymal type. Inhibition of this transition through targeting of specific mediators may be a useful supplementary strategy to circumvent the effects of loss of endocrine sensitivity.
We used microarrays to detail the global programme of gene expression underlying Epithelial to mesenchymal transition and identified distinct classes of regulated genes during this process.
 
Overall design MCF7 cell line was selected before and after (PII) silencing of Estrogen receptor for RNA extraction and hybridization on Affymetrix expression microarrays.
 
Contributor(s) Al-Mulla F, Lugmani Y
Citation(s) 21713035
Submission date Feb 23, 2011
Last update date Mar 25, 2019
Contact name fahd Al-Mulla
E-mail(s) fahd@al-mulla.org
Phone +96524986233
Organization name Kuwait University
Department Pathology
Lab Molecular pathology
Street address Faculty of medicine
City Kuwait
ZIP/Postal code 13110
Country Kuwait
 
Platforms (1)
GPL570 [HG-U133_Plus_2] Affymetrix Human Genome U133 Plus 2.0 Array
Samples (6)
GSM678802 MCF7, biological rep1
GSM678803 MCF7, biological rep2
GSM678804 MCF7, biological rep3
Relations
BioProject PRJNA138447

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Supplementary file Size Download File type/resource
GSE27473_RAW.tar 30.7 Mb (http)(custom) TAR (of CEL)
Raw data provided as supplementary file
Processed data included within Sample table

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