http://purl.uniprot.org/citations/17570496 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/17570496 | http://www.w3.org/2000/01/rdf-schema#comment | "BackgroundProliferative inflammatory atrophy (PIA) in the prostate has been proposed to be a precursor to prostate cancer. CCAAT/enhancer-binding protein beta (C/EBPbeta) is an important transcription factor involved in cellular proliferation and differentiation. Activation of C/EBPbeta plays a crucial role during the initial stage of cyclo-oxygenase 2 (COX-2) induction by proinflammatory mediators. Overexpression of C/EBPbeta has been reported in several human tumors. Nevertheless, the C/EBPbeta expression and functions in human prostate tissue are basically unknown.MethodsC/EBPbeta immunohistochemical staining was performed on 45 benign prostate hyperplasia (BPH) samples. The expression of C/EBPbeta in PIA lesions and normal-appearing acini was analyzed. In addition, by using double-IHC staining, C/EBPbeta expression and the association with chronic inflammatory cell density, co-expression of COX-2 and androgen receptor (AR) were also investigated.ResultsC/EBPbeta was occasionally observed in normal-appearing prostate acini (4.9% +/- 6.7%, Mean +/-SD) but was clearly overexpressed in PIA lesions (81.8% +/-16.4%) (P < 0.0001). Atrophic glands with T-lymphocyte and macrophage inflammation expressed higher level of C/EBPbeta. Furthermore, C/EBPbeta correlated significantly with COX-2 expression. Downregulation of the AR was common in PIA and was also related to the C/EBPbeta overexpression.ConclusionsThe data demonstrated that chronic inflammation appeared to play roles in the induction of C/EBPbeta expression in prostate epithelium, which was in turn associated with increased COX-2 expression and AR downregulation. In combining with other molecular alteration in the epithelium of PIA, it is suggested that these cells might be a kind of intermediate cells and involved in the pathogenesis of prostate cancer."xsd:string |
http://purl.uniprot.org/citations/17570496 | http://purl.org/dc/terms/identifier | "doi:10.1002/pros.20595"xsd:string |
http://purl.uniprot.org/citations/17570496 | http://purl.uniprot.org/core/author | "Wang W."xsd:string |
http://purl.uniprot.org/citations/17570496 | http://purl.uniprot.org/core/author | "Bergh A."xsd:string |
http://purl.uniprot.org/citations/17570496 | http://purl.uniprot.org/core/author | "Damber J.E."xsd:string |
http://purl.uniprot.org/citations/17570496 | http://purl.uniprot.org/core/date | "2007"xsd:gYear |
http://purl.uniprot.org/citations/17570496 | http://purl.uniprot.org/core/name | "Prostate"xsd:string |
http://purl.uniprot.org/citations/17570496 | http://purl.uniprot.org/core/pages | "1238-1246"xsd:string |
http://purl.uniprot.org/citations/17570496 | http://purl.uniprot.org/core/title | "Increased expression of CCAAT/enhancer-binding protein beta in proliferative inflammatory atrophy of the prostate: relation with the expression of COX-2, the androgen receptor, and presence of focal chronic inflammation."xsd:string |
http://purl.uniprot.org/citations/17570496 | http://purl.uniprot.org/core/volume | "67"xsd:string |
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