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This Article Full Text Full Text (PDF) All Versions of this Article: JME-08-0088v1 42/1/19    most recent Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Wu, F. Articles by Safe, S. Search for Related Content PubMed PubMed Citation Articles by Wu, F. Articles by Safe, S.

¹ Department of Biochemistry and Biophysics, Texas A&M University, College Station, Texas 77843, USA² Department of Veterinary Physiology and Pharmacology, Texas A&M University, 4466 TAMU, Veterinary Research Building 410, College Station, Texas 77843-4466, USA³ Institute of Biosciences and Technology, Texas A&M University Health Science Center, Houston, Texas 77030, USA

(Correspondence should be addressed to S Safe; Email: ssafe{at}cvm.tamu.edu)

17β-Estradiol (E₂) binds estrogen receptor (ESR1) in MCF-7 cells and increases cell proliferation and survival through induction or repression of multiple genes. ESR1 interactions with DNA-bound specificity protein (SP) transcription factors is a nonclassical genomic estrogenic pathway and the role of SP transcription factors in mediating hormone-dependent activation or repression of genes in MCF-7 cells was investigated by microarrays and RNA interference. MCF-7 cells were transfected with a nonspecific oligonucleotide or a cocktail of small inhibitory RNAs (iSP), which knockdown SP1, SP3, and SP4 proteins, and treated with dimethylsulfoxide or 10 nM E₂ for 6 h. E₂ induced 62 and repressed 134 genes and the induction or repression was reversed in 62% of the genes in cells transfected with iSP (ESR1/SP dependent), whereas hormonal activation or repression of the remaining genes was unaffected by iSP (SP independent). Analysis of the ESR1/SP-dependent and SP-independent genes showed minimal overlap with respect to the GO terms (functional processes) in genes induced or repressed, suggesting that the different genomic pathways may contribute independently to the hormone-induced phenotype in MCF-7 cells.