NF-ĸβ upregulates ADAMTS5 expression by direct binding after TNF-α treatment in OUMS-27 chondrosarcoma cell line

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dc.contributor.authorGun Bilgic D.
dc.contributor.authorHatipoglu O.F.
dc.contributor.authorCigdem S.
dc.contributor.authorBilgic A.
dc.contributor.authorCora T.
dc.date.accessioned2024-07-22T08:07:16Z
dc.date.available2024-07-22T08:07:16Z
dc.date.issued2020
dc.description.abstractInflammation caused-aggrecan degradation is a critical event in the pathogenesis of osteoarthritis (OA). The aggrecanases like a disintegrin and metalloproteinase with thrombospondin motifs 5 (ADAMTS5) are assumed to be key players in the aggrecan destruction. To develop the comprehensive therapy method for OA, it is essential to elucidate the activation mechanism of ADAMTS5 gene after stimulation of inflammatory cytokines like tumor necrosis factor-α (TNF-α). The cell lines of human chondrosarcoma (OUMS-27) and embryonic kidney (HEK293T) were incubated with tumor necrosis factor-α (TNF-α) for certain time periods, and the expression level of ADAMTS5 was measured in both mRNA and protein levels. Tissue-specific ADAMTS5 activation was founded to be induced after TNF-α treatment. Then, the constructs for the promoter region of ADAMTS5 were prepared and luciferase assay was conducted to understand the involvement mechanism of nuclear factor-kappa beta (NF-ĸβ) in ADAMTS5 activation. It was demonstrated that NF-ĸβ induces the ADAMTS5 expression level by directly binding the promoter region of ADAMTS5. Although the TNF-α blocker is used for OA treatment, the development of a more comprehensive treatment strategy is an urgent need. Our experimental data contributes in terms of selecting NF-ĸβ as a target molecule. Up to date, NF-ĸβ has been proven to involve in the ADAMTS5 up-regulation after several pro-inflammatory cytokines stimulation. In conclusion, our findings make important contributions to the knowledge about the roles of NF-ĸβ in ADAMTS5 activation under inflammatory conditions. So, NF-ĸβ could be considered to be a potential target for OA treatment. © 2020, Springer Nature B.V.
dc.identifier.DOI-ID10.1007/s11033-020-05514-3
dc.identifier.issn03014851
dc.identifier.urihttp://akademikarsiv.cbu.edu.tr:4000/handle/123456789/13883
dc.language.isoEnglish
dc.publisherSpringer
dc.subjectADAMTS5 Protein
dc.subjectBone Neoplasms
dc.subjectCell Line, Tumor
dc.subjectChondrocytes
dc.subjectChondrosarcoma
dc.subjectHEK293 Cells
dc.subjectHumans
dc.subjectInterleukin-1beta
dc.subjectNF-kappa B
dc.subjectNF-KappaB Inhibitor alpha
dc.subjectOsteoarthritis
dc.subjectSignal Transduction
dc.subjectTranscriptional Activation
dc.subjectTumor Necrosis Factor-alpha
dc.subjectaggrecanase 2
dc.subjectI kappa B kinase alpha
dc.subjectimmunoglobulin enhancer binding protein
dc.subjectmessenger RNA
dc.subjecttumor necrosis factor
dc.subjectADAMTS5 protein, human
dc.subjectaggrecanase 2
dc.subjectI kappa B kinase alpha
dc.subjectimmunoglobulin enhancer binding protein
dc.subjectinterleukin 1beta
dc.subjecttumor necrosis factor
dc.subjectADAMTS5 gene
dc.subjectArticle
dc.subjectcontrolled study
dc.subjectembryo
dc.subjectgene activation
dc.subjectHEK293T cell line
dc.subjecthuman
dc.subjecthuman cell
dc.subjectosteoarthritis
dc.subjectOUMS-27 cell line
dc.subjectpromoter region
dc.subjectprotein expression
dc.subjectprotein protein interaction
dc.subjectupregulation
dc.subjectbiosynthesis
dc.subjectbone tumor
dc.subjectchondrocyte
dc.subjectchondrosarcoma
dc.subjectdrug effect
dc.subjectgenetics
dc.subjectHEK293 cell line
dc.subjectmetabolism
dc.subjectosteoarthritis
dc.subjectsignal transduction
dc.subjecttranscription initiation
dc.subjecttumor cell line
dc.titleNF-ĸβ upregulates ADAMTS5 expression by direct binding after TNF-α treatment in OUMS-27 chondrosarcoma cell line
dc.typeArticle

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