<?xml version="1.0" encoding="UTF-8"?><xml><records><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Bouris, P.</style></author><author><style face="normal" font="default" size="100%">Skandalis, S. S.</style></author><author><style face="normal" font="default" size="100%">Piperigkou, Z.</style></author><author><style face="normal" font="default" size="100%">Afratis, N.</style></author><author><style face="normal" font="default" size="100%">Karamanou, K.</style></author><author><style face="normal" font="default" size="100%">Aletras, A. J.</style></author><author><style face="normal" font="default" size="100%">Moustakas, A.</style></author><author><style face="normal" font="default" size="100%">Theocharis, A. D.</style></author><author><style face="normal" font="default" size="100%">Karamanos, N. K.</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Estrogen receptor alpha mediates epithelial to mesenchymal transition, expression of specific matrix effectors and functional properties of breast cancer cells</style></title><secondary-title><style face="normal" font="default" size="100%">Matrix BiolMatrix Biol</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">*Epithelial-Mesenchymal Transition</style></keyword><keyword><style  face="normal" font="default" size="100%">breast cancer</style></keyword><keyword><style  face="normal" font="default" size="100%">Breast Neoplasms/genetics/metabolism/*pathology</style></keyword><keyword><style  face="normal" font="default" size="100%">Cell Movement</style></keyword><keyword><style  face="normal" font="default" size="100%">Cell Proliferation</style></keyword><keyword><style  face="normal" font="default" size="100%">EGFR</style></keyword><keyword><style  face="normal" font="default" size="100%">Epithelial to mesenchymal transition</style></keyword><keyword><style  face="normal" font="default" size="100%">estrogen receptor</style></keyword><keyword><style  face="normal" font="default" size="100%">Estrogen Receptor alpha/*genetics/metabolism</style></keyword><keyword><style  face="normal" font="default" size="100%">Extracellular Matrix/genetics/*metabolism</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Gene Expression Regulation, Neoplastic</style></keyword><keyword><style  face="normal" font="default" size="100%">Gene Knockdown Techniques</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Invasion</style></keyword><keyword><style  face="normal" font="default" size="100%">Matrix metalloproteinases</style></keyword><keyword><style  face="normal" font="default" size="100%">MCF-7 Cells</style></keyword><keyword><style  face="normal" font="default" size="100%">Migration</style></keyword><keyword><style  face="normal" font="default" size="100%">tPA</style></keyword><keyword><style  face="normal" font="default" size="100%">uPA</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2015</style></year><pub-dates><date><style  face="normal" font="default" size="100%">Apr</style></date></pub-dates></dates><edition><style face="normal" font="default" size="100%">20150227</style></edition><volume><style face="normal" font="default" size="100%">43</style></volume><pages><style face="normal" font="default" size="100%">42-60</style></pages><isbn><style face="normal" font="default" size="100%">1569-1802 (Electronic)0945-053X (Linking)</style></isbn><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">The 17beta-estradiol (E2)/estrogen receptor alpha (ERalpha) signaling pathway is one of the most important pathways in hormone-dependent breast cancer. E2 plays pivotal roles in cancer cell growth, survival, and architecture as well as in gene expression regulatory mechanisms. In this study, we established stably transfected MCF-7 cells by knocking down the ERalpha gene (designated as MCF-7/SP10+ cells), using specific shRNA lentiviral particles, and compared them with the control cells (MCF-7/c). Interestingly, ERalpha silencing in MCF-7 cells strongly induced cellular phenotypic changes accompanied by significant changes in gene and protein expression of several markers typical of epithelial to mesenchymal transition (EMT). Notably, these cells exhibited enhanced cell proliferation, migration and invasion. Moreover, ERalpha suppression strongly affected the gene and protein expression of EGFR and HER2 receptor tyrosine kinases, and various extracellular matrix (ECM) effectors, including matrix metalloproteinases and their endogenous inhibitors (MMPs/TIMPs) and components of the plasminogen activation system. The action caused by E2 in MCF-7/c cells in the expression of HER2, MT1-MMP, MMP1, MMP9, uPA, tPA, and PAI-1 was abolished in MCF-7/SP10+ cells lacking ERalpha. These data suggested a regulatory role for the E2/ERalpha pathway in respect to the composition and activity of the extracellular proteolytic molecular network. Notably, loss of ERalpha promoted breast cancer cell migration and invasion by inducing changes in the expression levels of certain matrix macromolecules (especially uPA, tPA, PAI-1) through the EGFR-ERK signaling pathway. In conclusion, loss of ERalpha in breast cancer cells results in a potent EMT characterized by striking changes in the expression profile of specific matrix macromolecules highlighting the potential nodal role of matrix effectors in breast cancer endocrine resistance.</style></abstract><accession-num><style face="normal" font="default" size="100%">25728938</style></accession-num><notes><style face="normal" font="default" size="100%">Bouris, PanagiotisSkandalis, Spyros SPiperigkou, ZoiAfratis, NikosKaramanou, KonstantinaAletras, Alexios JMoustakas, AristidisTheocharis, Achilleas DKaramanos, Nikos KengResearch Support, Non-U.S. Gov'tNetherlands2015/03/03Matrix Biol. 2015 Apr;43:42-60. doi: 10.1016/j.matbio.2015.02.008. Epub 2015 Feb 27.</style></notes><auth-address><style face="normal" font="default" size="100%">Biochemistry, Biochemical Analysis &amp; Matrix Pathobiology Res. Group, Laboratory of Biochemistry, Department of Chemistry, University of Patras, Patras 26110, Greece.Biochemistry, Biochemical Analysis &amp; Matrix Pathobiology Res. Group, Laboratory of Biochemistry, Department of Chemistry, University of Patras, Patras 26110, Greece; Universite de Reims Champagne Ardenne, Laboratoire de Biochimie Medicale et de Biologie Moleculaire, Reims, France.Department of Medical Biochemistry and Microbiology, Ludwig Institute for Cancer Research, Science for Life Laboratory, Uppsala University, Box 582, SE 751 23 Uppsala, Sweden.Biochemistry, Biochemical Analysis &amp; Matrix Pathobiology Res. Group, Laboratory of Biochemistry, Department of Chemistry, University of Patras, Patras 26110, Greece. Electronic address: n.k.karamanos@upatras.gr.</style></auth-address><remote-database-name><style face="normal" font="default" size="100%">Medline</style></remote-database-name><remote-database-provider><style face="normal" font="default" size="100%">NLM</style></remote-database-provider></record></records></xml>