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<biogps><data><item key="owner">ArrayExpress Uploader</item><item key="pop_total">0</item><item key="id">1446</item><item key="factors"><item><item key="GSE4006GSM91267"><item key="GENETICMODIFICATION">AdERb low moi</item><item key="COMPOUND">17beta-estradiol</item></item></item><item><item key="GSE4006GSM91262"><item key="GENETICMODIFICATION">empty adenovirus</item><item key="COMPOUND">17beta-estradiol</item></item></item><item><item key="GSE4006GSM91269"><item key="GENETICMODIFICATION">AdERb high moi</item><item key="COMPOUND">control</item></item></item><item><item key="GSE4006GSM91260"><item key="GENETICMODIFICATION">empty adenovirus</item><item key="COMPOUND">control</item></item></item><item><item key="GSE4006GSM91260"><item key="GENETICMODIFICATION">empty adenovirus</item><item key="COMPOUND">control</item></item></item><item><item key="GSE4006GSM91269"><item key="GENETICMODIFICATION">AdERb high moi</item><item key="COMPOUND">control</item></item></item><item><item key="GSE4006GSM91270"><item key="GENETICMODIFICATION">AdERb high moi</item><item key="COMPOUND">17beta-estradiol</item></item></item><item><item key="GSE4006GSM91267"><item key="GENETICMODIFICATION">AdERb low moi</item><item key="COMPOUND">17beta-estradiol</item></item></item><item><item key="GSE4006GSM91265"><item key="GENETICMODIFICATION">AdERb low moi</item><item key="COMPOUND">control</item></item></item><item><item key="GSE4006GSM91270"><item key="GENETICMODIFICATION">AdERb high moi</item><item key="COMPOUND">17beta-estradiol</item></item></item><item><item key="GSE4006GSM91262"><item key="GENETICMODIFICATION">empty adenovirus</item><item key="COMPOUND">17beta-estradiol</item></item></item><item><item key="GSE4006GSM91265"><item key="GENETICMODIFICATION">AdERb low moi</item><item key="COMPOUND">control</item></item></item></item><item key="ownerprofile_id">arrayexpress_sid</item><item key="platform">3</item><item key="summary_wrapped">Two subtypes of the estrogen receptor, ERalpha and ERbeta, mediate the actions of estrogens, and the majority of human breast tumors...</item><item key="pubmed_id">16809442</item><item key="geo_gse_id">E-GEOD-4006</item><item key="owner_profile">/profile/8773/arrayexpressuploader</item><item key="factor_count">2</item><item key="sample_count">12</item><item key="tags"><item>breast</item><item>breast cancer</item><item>cancer</item><item>estrogen</item><item>genome</item></item><item key="lastmodified">Dec.12, 2014</item><item key="is_default">False</item><item key="geo_gds_id"/><item key="slug">transcription-profiling-of-human-cancer-cell-line</item><item key="geo_id_plat">E-GEOD-4006_A-AFFY-33</item><item key="name">Transcription profiling of human cancer cell line MCF-7  - estrogen effects where MCF7 is co-expressing ERa and ERb</item><item key="created">Jun.19, 2014</item><item key="summary">Two subtypes of the estrogen receptor, ERalpha and ERbeta, mediate the actions of estrogens, and the majority of human breast tumors contain both ERalpha and ERbeta. To examine the possible interactions and modulatory effects of ERbeta on ERalpha activity, we have used adenoviral gene delivery to produce human breast cancer (MCF-7) cells expressing ERbeta, along with their endogenous ERalpha. We have examined the effects of ER&#946; expression on genome-wide gene expression by Affymetrix GeneChip microarrays. We find that ERbeta modulated estrogen gene expression on nearly 24% of E2-stimulated genes but only 8% of E2-inhibited genes. We find that ERbeta modulation is gene-specific, enhancing or counteracting ERalpha regulation for distinct subsets of estrogen target genes.  Introduction of ERbeta into ERalpha-containing cells induced up/down-regulation of many estrogen target in the absence of any added ligand.  In addition, ERbeta presence elicited the expression of a unique set of genes that were not regulated by ERalpha alone.  ERbeta modulated the expression of genes in many functional categories, but the greatest numbers were associated with transcription factor and signal transduction pathways. Regulation of multiple components in the TGF beta, SDF1, and semaphorin pathways, may contribute to the suppression of proliferation observed with ERbeta both in the presence and absence of estrogen. Hence, ERbeta modulates ERalpha gene regulation in diverse ways that may contribute to its growth-inhibiting beneficial effects in breast cancer Experiment Overall Design: MCF-7 cells expressing endogenous ERalpha were infected with adenovirus carrying either estrogen receptor beta (AdERb) or no insert (Ad) at multiplicity of infection (moi) of 5 or 50.  Cells were infected with adenovirus for a period of 48hr before treatment with ligand (vehicle control or 10nM 17beta-estradiol) for a additional period of 24hr before harvest.</item><item key="source">http://www.ebi.ac.uk/arrayexpress/experiments/E-GEOD-4006</item><item key="species">human</item><item key="sample_source">http://www.ebi.ac.uk/arrayexpress/experiments/E-GEOD-4006/samples/</item></data></biogps>
