Interleukin-1 induced nuclear factor-B binds to a disintegrin-like and metalloproteinase with thrombospondin type 1 motif 9 promoter in human chondrosarcoma cells

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dc.authoridoskay halacli, sevil/0000-0003-1101-1779
dc.contributor.authorAltuntas, Aynur
dc.contributor.authorHalacli, Sevil Oskay
dc.contributor.authorCakmak, Ozlem
dc.contributor.authorErden, Gonul
dc.contributor.authorAkyol, Sumeyya
dc.contributor.authorUgurcu, Veli
dc.contributor.authorHirohata, Satoshi
dc.date.accessioned2025-10-24T18:09:47Z
dc.date.available2025-10-24T18:09:47Z
dc.date.issued2015
dc.departmentMalatya Turgut Özal Üniversitesi
dc.description.abstractNuclear factor-B (NF-B) is involved in the regulation of inflammation-associated genes. NF-B forms dimers which bind with sequences referred to as NF-B sites (9-11 bp). A disintegrin-like and metalloproteinase with thrombospondin type 1 motif 9 (ADAMTS9) is a type of proteoglycanase, which proteolytically cleaves versican and aggrecan. ADAMTS9 is a cytokine-inducible gene that contains binding sites for NF-B within its promoter region. Interleukin-1 (IL-1) affects cartilage metabolism and is involved in the NF-B pathway. It is therefore hypothesized that NF-B binding with ADAMTS9 promoters may activate IL-1, thereby promoting chondrocytic cell growth. In the present study, the OUMS-27 chondrocytic human chondrosarcoma cell line was treated with IL-1 with or without inhibitors of NF-B signaling pathways. Chromatin immunoprecipitation (ChIP) and electromobility shift assays (EMSA) were conducted order to analyze the binding of NF-B with the ADAMTS9 promoter region. NF-B-p65 subunit phosphorylation was promoted in IL-1-treated cells, which were not treated with inhibitors of NF-B signaling pathways. By contrast, NF-B-p65 subunit phosphorylation was inhibited in cells that had been treated with BAY-117085, an NF-B pathway inhibitor. ChIP and EMSA assays demonstrated that, following treatment with IL-1, NF-B-p65 bound to elements located at -1177 and -1335 in the ADAMTS9 promoter region, in contrast to the untreated samples. The results of the present study suggested that NF-B may be involved in IL-1-induced activation of ADAMTS9 in human chondrocytes.
dc.description.sponsorshipGrants-in-Aid for Scientific Research [26670665] Funding Source: KAKEN
dc.identifier.doi10.3892/mmr.2015.3444
dc.identifier.endpage600
dc.identifier.issn1791-2997
dc.identifier.issn1791-3004
dc.identifier.issue1
dc.identifier.pmid25760020
dc.identifier.scopus2-s2.0-84926675424
dc.identifier.scopusqualityQ1
dc.identifier.startpage595
dc.identifier.urihttps://doi.org/10.3892/mmr.2015.3444
dc.identifier.urihttps://hdl.handle.net/20.500.12899/3831
dc.identifier.volume12
dc.identifier.wosWOS:000358134400086
dc.identifier.wosqualityQ3
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherSpandidos Publ Ltd
dc.relation.ispartofMolecular Medicine Reports
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/openAccess
dc.snmzKA_20251023
dc.subjecta disintegrin-like and metalloproteinase with thrombospondin type 1 motif 9; nuclear factor-B; interleukin-1
dc.titleInterleukin-1 induced nuclear factor-B binds to a disintegrin-like and metalloproteinase with thrombospondin type 1 motif 9 promoter in human chondrosarcoma cells
dc.title.alternativeInterleukin-1? induced nuclear factor-?B binds toa disintegrin-like and metalloproteinase with thrombospondin type 1 motif 9 promoter in human chondrosarcoma cells
dc.typeArticle

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