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dc.creatorMitrović-Ajtić, Olivera
dc.creatorSubotički, Tijana
dc.creatorDiklić, Miloš
dc.creatorĐikić, Dragoslava
dc.creatorVukotić, Milica
dc.creatorDragojević, Teodora
dc.creatorŽivković, Emilija
dc.creatorAntić, Darko
dc.creatorČokić, Vladan
dc.date.accessioned2022-07-22T12:49:42Z
dc.date.available2022-07-22T12:49:42Z
dc.date.issued2022
dc.identifier.issn1422-0067
dc.identifier.urihttp://rimi.imi.bg.ac.rs/handle/123456789/1244
dc.description.abstractThe calcium-binding proteins S100A4, S100A8, and S100A9 are upregulated in chronic lymphocytic leukemia (CLL), while the S100A9 promotes NF-κB activity during disease progression. The S100-protein family has been involved in several malignancies as mediators of inflammation and proliferation. The hypothesis of our study is that S100A proteins are mediators in signaling pathways associated with inflammation-induced proliferation, such as NF-κB, PI3K/AKT, and JAK/STAT. The mononuclear cells (MNCs) of CLL were treated with proinflammatory IL-6, anti-inflammatory IL-10 cytokines, inhibitors of JAK1/2, NF-κB, and PI3K signaling pathways, to evaluate S100A4, S100A8, S100A9, and S100A12 expression as well as NF-κB activation by qRT-PCR, immunocytochemistry, and immunoblotting. The quantity of S100A4, S100A8, and S100A9 positive cells (p < 0.05) and their protein expression (p < 0.01) were significantly decreased in MNCs of CLL patients compared to healthy controls. The S100A levels were generally increased in CD19+ cells compared to MNCs of CLL. The S100A4 gene expression was significantly stimulated (p < 0.05) by the inhibition of the PI3K/AKT signaling pathway in MNCs. IL-6 stimulated S100A4 and S100A8 protein expression, prevented by the NF-κB and JAK1/2 inhibitors. In contrast, IL-10 reduced S100A8, S100A9, and S100A12 protein expressions in MNCs of CLL. Moreover, IL-10 inhibited activation of NF-κB signaling (4-fold, p < 0.05). In conclusion, inflammation stimulated the S100A protein expression mediated via the proliferation-related signaling and balanced by the cytokines in CLL.
dc.publisherMDPI
dc.relationinfo:eu-repo/grantAgreement/MESTD/inst-2020/200015/RS//
dc.rightsopenAccess
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/
dc.sourceInternational Journal of Molecular Sciences
dc.subjectinflammation
dc.subjectIL-6
dc.subjectIL-10
dc.subjectCLL
dc.subjectprognostic markers
dc.titleRegulation of S100As Expression by Inflammatory Cytokines in Chronic Lymphocytic Leukemia
dc.typearticle
dc.rights.licenseBY
dc.citation.issue13
dc.citation.spage6952
dc.citation.volume23
dc.identifier.doi10.3390/ijms23136952
dc.identifier.fulltexthttp://rimi.imi.bg.ac.rs/bitstream/id/2775/Regulation_of_S100As_Expression_by_Inflammatory_Cytokines_pub_2022.pdf
dc.type.versionpublishedVersion


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