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• W2433363072 abstract "// Erika Terzuoli 1, * , Sandra Donnini 1, 2, * , Federica Finetti 1 , Gabriella Nesi 3 , Donata Villari 4 , Hiromi Hanaka 5 , Olof Radmark 5 , Antonio Giachetti 1 , Marina Ziche 1, 2 1 Department of Life Sciences, University of Siena, 53100, Siena, Italy 2 Istituto Toscano Tumori (ITT), 50136, Florence, Italy 3 Department of Surgery and Translational Medicine, University of Florence, 50136, Florence, Italy 4 Department of Clinical and Experimental Medicine, University of Florence, 50136, Florence, Italy 5 Department of Medical Biochemistry and Biophysics, Karolinska Institutet, S-171 77, Stockholm, Sweden * These authors contributed equally to this work Correspondence to: Marina Ziche, email: marina.ziche@unisi.it Keywords: miR-186, mPGES-1/PGE-2, VEGF, prostate cancer, tumor angiogenesis Received: January 12, 2016      Accepted: June 01, 2016      Published: June 14, 2016 ABSTRACT Prostaglandin E-2 (PGE-2) promotes tumor angiogenesis via paracrine secretion of pro-angiogenic growth factors, such as vascular endothelial growth factor (VEGF). Since miRNAs regulate several cell processes, including angiogenesis, we sought to determine whether they would influence PGE-2-induced VEGF. We compared DU145 and PC3 prostate cancer cells bearing the mPGES-1 enzyme (mPGES-1 +/+ ) and producing PGE-2, with those in which the enzyme was silenced or deleted (mPGES-1 -/- ). We demonstrated that mPGES-1/PGE-2 signaling decreased Dicer expression and miRNA biogenesis. Genome-wide sequencing of miRNAs revealed that miR-15a and miR-186, associated with expression of VEGF and hypoxia inducible factor-1α (HIF-1α), were down-regulated in mPGES-1 +/+ cells. As a consequence, mPGES-1 +/+ tumor cells expressed high levels of VEGF and HIF-1α, induced endothelial cells activation and formed highly vascularized tumors. Mir-186 mimic inhibited VEGF expression in mPGES-1 +/+ tumor xenografts and reduced tumor growth. In human prostate cancer specimens, mPGES-1 was over-expressed in tumors with high Gleason score, elevated expression of VEGF and HIF-1α, high microvessel density and decreased expression of Dicer, miR15a and miR-186. Thus, clear evidence for regulating miRNA processing and VEGF output by intrinsic PGE-2 production provides a means to distinguish between aggressive and indolent prostate tumors and suggests a potential target for controlling tumor progression." @default.
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• W2433363072 date "2016-06-14" @default.
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• W2433363072 title "Linking microsomal prostaglandin E Synthase-1/PGE-2 pathway with miR-15a and −186 expression: Novel mechanism of VEGF modulation in prostate cancer" @default.
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• W2433363072 doi "https://doi.org/10.18632/oncotarget.10051" @default.
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