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Series GSE80366 Query DataSets for GSE80366
Status Public on Jun 01, 2016
Title Genomic agonism and phenotypic antagonism between estrogen and progesterone receptors in breast cancer. [cell models RNA-seq]
Organism Homo sapiens
Experiment type Expression profiling by high throughput sequencing
Summary Transcriptomic changes and estrogen and progesterone receptor binding in multiple ER+/PR+ models (eight ER+/PR+ patient tumors, various T47Ds, ZR75) and multiple ER+/PR-negative models (four ER+/PR- patient tuumors, PR-deficient T47D and MCF7 cells) treated with various hormone combinations.
Results: In isolation, estrogen and progestin act as genomic agonists by regulating the expression of common target genes in similar directions, but at different levels. Similarly, in isolation, progestin is also a weak phenotypic agonist of estrogen action. However, in the presence of both hormones, progestin behaves as a phenotypic estrogen antagonist. PR remodels nucleosomes to noncompetitively redirect ER genomic binding to distal enhancers enriched for BRCA1 binding motifs and sites that link PR and ER/PR complexes. Importantly, when both hormones are present, progestin modulates estrogen action such that responsive transcriptomes, cellular processes and ER/PR recruitment to genomic sites correlate with those observed with PR alone, but not ER alone.
Conclusions: Genomic Agonism and Phenotypic Antagonism between Estrogen and Progesterone Receptors in Breast Cancer. Individual and concerted actions of ER and PR highlight the prognostic and therapeutic value of PR in ER+/PR+ breast cancers.
 
Overall design ER+/PR+ and ER+/PR-deficient model systems were deprived of steroids by culturing them in phenol red free RPMI 1640 media that is supplemented with 10% charcoal-stripped fetal bovine serum and 1% penicillin/streptomycin. Subsequently, these steroid-deprived models were treated with either vehicle, 10 nM estradiol, 10 nM progestin R5020 or 10 nM of both the hormones and genomics (ChIP-seq and RNA-seq) was performed. ChIP-seq was done after 45 minutes of hormone treatments. For cell models, RNA-seq was done after 12 hours of hormone treatments. Tumor explants were treated with either 24 or 48 hours.
 
Contributor(s) Greene G, Singhal H
Citation(s) 27386569
Submission date Apr 18, 2016
Last update date May 15, 2019
Contact name Hari Singhal
E-mail(s) [email protected]
Organization name University of Chicago
Department Ben May Department for Cancer Research
Lab Geoffrey L Greene
Street address 929 E 57th St
City Chicago
State/province IL
ZIP/Postal code 60637
Country USA
 
Platforms (1)
GPL16791 Illumina HiSeq 2500 (Homo sapiens)
Samples (28)
GSM2112767 Cells_T47D_Vehicle_12 Hours_RNAseq
GSM2112768 Cells_T47D_E2_12 Hours_RNAseq
GSM2112769 Cells_T47D_R5020_12 Hours_RNAseq
This SubSeries is part of SuperSeries:
GSE80098 Genomic agonism and phenotypic antagonism between estrogen and progesterone receptors in breast cancer.
Relations
BioProject PRJNA318945

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Supplementary file Size Download File type/resource
GSE80366_MCF7_RNAseq.csv.gz 83.8 Kb (ftp)(http) CSV
GSE80366_PR-deficient_T47D_RNAseq.csv.gz 35.1 Kb (ftp)(http) CSV
GSE80366_T47D_RNAseq.csv.gz 153.9 Kb (ftp)(http) CSV
GSE80366_T47D_siControl_RNAseq.csv.gz 67.5 Kb (ftp)(http) CSV
GSE80366_T47D_siFOXA1_annotated100kb_RNAseq.csv.gz 20.5 Kb (ftp)(http) CSV
GSE80366_T47D_siNF1C_RNAseq.csv.gz 49.3 Kb (ftp)(http) CSV
GSE80366_ZR75_RNAseq.csv.gz 84.8 Kb (ftp)(http) CSV
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Raw data provided as supplementary file
Processed data are available on Series record
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