Please use this identifier to cite or link to this item: https://hdl.handle.net/11147/5572
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dc.contributor.authorDebeleç Bütüner, Bilge-
dc.contributor.authorAlapınar, Cansu-
dc.contributor.authorVarışlı, Lokman-
dc.contributor.authorErbaykent Tepedelen, Burcu-
dc.contributor.authorHamid, Syed Muhammad-
dc.contributor.authorGönen Korkmaz, Ceren-
dc.contributor.authorKorkmaz, Kemal Sami-
dc.date.accessioned2017-05-23T06:54:52Z
dc.date.available2017-05-23T06:54:52Z
dc.date.issued2014-02
dc.identifier.citationDebeleç Bütüner, B., Alapınar, C., Varışlı, L., Erbaykent Tepedelen, B., Hamid, S. M., Gönen Korkmaz, C., and Korkmaz, K.S. (2014). Inflammation-mediated abrogation of androgen signaling: An in vitro model of prostate cell inflammation. Molecular Carcinogenesis, 53(29), 85-97. doi:10.1002/mc.21948en_US
dc.identifier.issn0899-1987
dc.identifier.issn0899-1987-
dc.identifier.issn1098-2744-
dc.identifier.urihttps://doi.org/10.1002/mc.21948
dc.identifier.urihttp://hdl.handle.net/11147/5572
dc.description.abstractAs a link between inflammation and cancer has been reported in many studies, we established an in vitro model of prostatic inflammation to investigate the loss of androgen receptor (AR)-mediated signaling in androgen responsive prostate cell lines. First, the U937 monocyte cell line was differentiated into macrophages using phorbol acetate (PMA), and cells were induced with lipopolysaccharide (LPS) for cytokine secretion. Next, the cytokine levels (TNFα, IL-6, and IL1β) in conditioned media (CM) were analyzed. Prostate cells were then fed with CM containing varying concentrations of TNFα, and IkB degradation, nuclear factor kappa B (NFκB) translocation and transactivation, and the expression of matrix metalloproteinase-8 (MMP8) and matrix metalloproteinase-9 (MMP9) were then assessed. As a result of CM treatment, ubiquitin-mediated AR degradation, which was restored using anti-TNFα antibody neutralization, led to both a decrease in KLK4, PSA, and NKX3.1 expression levels and the upregulation of GPX2. In addition to the loss of AR, acute and chronic CM exposure resulted in p53 degradation and consequent p21 downregulation, which was also restored by either androgen administration or ectopic NKX3.1 expression via the stabilization of MDM2 levels in LNCaP cells. Additionally, CM treatment enhanced H2AX(S139) phosphorylation (a hallmark of DNA damage) and genetic heterogeneity in the absence of androgens in prostate cells without activating mitochondrial apoptosis. Thus, the data suggest that inflammatory cytokine exposure results in the loss of AR and p53 signaling in prostate cells and facilitates genetic heterogeneity via ROS accumulation to promote prostate carcinogenesis.en_US
dc.description.sponsorshipTurkish Scientific and Technological Research Council (TUBITAK-106S200/TUBITAK-110S134/TUBITAK-108S288); COST action (BM0703 CANGENIN); Ege Universityen_US
dc.language.isoenen_US
dc.publisherJohn Wiley and Sons Inc.en_US
dc.relation.ispartofMolecular Carcinogenesisen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectAndrogenen_US
dc.subjectDNA damageen_US
dc.subjectInflammationen_US
dc.subjectLoss of p53en_US
dc.subjectProstate canceren_US
dc.titleInflammation-mediated abrogation of androgen signaling: An in vitro model of prostate cell inflammationen_US
dc.typeArticleen_US
dc.institutionauthorHamid, Syed Muhammad-
dc.departmentİzmir Institute of Technology. Molecular Biology and Geneticsen_US
dc.identifier.volume53en_US
dc.identifier.issue2en_US
dc.identifier.startpage85en_US
dc.identifier.endpage97en_US
dc.identifier.wosWOS:000329926900001en_US
dc.identifier.scopus2-s2.0-84892884295en_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.identifier.doi10.1002/mc.21948-
dc.identifier.pmid22911881en_US
dc.relation.doi10.1002/mc.21948en_US
dc.coverage.doi10.1002/mc.21948en_US
dc.identifier.scopusqualityQ2-
item.openairetypeArticle-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.fulltextWith Fulltext-
item.languageiso639-1en-
item.cerifentitytypePublications-
item.grantfulltextopen-
Appears in Collections:Molecular Biology and Genetics / Moleküler Biyoloji ve Genetik
PubMed İndeksli Yayınlar Koleksiyonu / PubMed Indexed Publications Collection
Scopus İndeksli Yayınlar Koleksiyonu / Scopus Indexed Publications Collection
WoS İndeksli Yayınlar Koleksiyonu / WoS Indexed Publications Collection
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