Estrogen receptor beta modulates breast cancer cells functional properties, signaling and expression of matrix molecules

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• 作者：Zoi Piperigkou^a ; ^b ; Panagiotis Bouris^a ; Maurizio Onisto^c ; Marco Franchi^d ; Dimitris Kletsas^e ; Achilleas D. Theocharis^a ; Nikos K. Karamanos^a ; ^b ; ^{n.k.karamanos@upatras.gr}
• 关键词：ECM ; extracellular matrix ; EGFR ; epidermal growth factor receptor ; EMT ; epithelial-to-mesenchymal-transition ; ER ; estrogen receptor ; ERK ; extracellular signal-regulated kinase ; ERE ; estrogen responsive element ; GAG ; glycosaminoglycan ; HSPG ; heparan sulfate proteoglycan ; HSPE ; heparanase ; IGF-IR ; insulin-like growth factor receptor type I ; MMP ; matrix metalloproteinase ; SDC ; syndecan ; TIMP ; tissue inhibitor of MMPs ; tPA ; tissue plasminogen activator ; uPA ; urokinase plasminogen activator
• 刊名：Matrix Biology
• 出版年：2016
• 出版时间：December 2016
• 年：2016
• 卷：56
• 期：Complete
• 页码：4-23
• 全文大小：2168 K
• 卷排序：56

文摘

ERβ suppression in breast cancer cells induces significant phenotypic changes and alters the expression of EMT markers. ERβ suppressed cells exhibit modified functional cell properties (proliferation, migration, invasion and adhesion). Migration is significantly reduced through the EGFR/IGF-IR and the JAK/STAT signaling pathways. ERβ modulates the gene expression of proteoglycans, matrix metalloproteinases and plasminogen activation system components. ERβ is a potential target to improve design of novel pharmaceuticals against aggressive breast cancer.