OGG1 as an epigenetic reader affects NF?B: What this means for cancer

Basit Öğe Kaydı
dc.authorid0000-0002-4337-9327en_US
dc.contributor.authorVlahopoulos, Spiros
dc.contributor.authorPan, Lang
dc.contributor.authorVarışli, Lokman
dc.contributor.authorDancik, Garrett M.
dc.contributor.authorKarantanos, Theodoros
dc.contributor.authorBoldogh, Istvan
dc.date.accessioned2024-01-18T12:47:57Z
dc.date.available2024-01-18T12:47:57Z
dc.date.issued2024en_US
dc.departmentDicle Üniversitesi, Fen Fakültesi, Moleküler Biyoloji ve Genetik Bölümüen_US
dc.description.abstract8-oxoguanine glycosylase 1 (OGG1), which was initially identified as the enzyme that catalyzes the first step in the DNA base excision repair pathway, is now also recognized as a modulator of gene expression. What is important for cancer is that OGG1 acts as a modulator of NFκB-driven gene expression. Specifically, oxidant stress in the cell transiently halts enzymatic activity of substrate-bound OGG1. The stalled OGG1 facilitates DNA binding of transactivators, such as NFκB to their cognate sites, enabling the expression of cytokines and chemokines, with ensuing recruitment of inflammatory cells. Recently, we highlighted chief aspects of OGG1 involvement in regulation of gene expression, which hold significance in lung cancer development. However, OGG1 has also been implicated in the molecular underpinning of acute myeloid leukemia. This review analyzes and discusses how these cells adapt through redox-modulated intricate connections, via interaction of OGG1 with NFκB, which provides malignant cells with alternative molecular pathways to transform their microenvironment, enabling adjustment, promoting cell proliferation, metastasis, and evading killing by therapeutic agents.en_US
dc.identifier.citationVlahopoulos, S., Pan, L., Varışli, L., Dancik, G. M., Karantanos, T. ve Boldogh, I. (2024). OGG1 as an epigenetic reader affects NFκB: What this means for cancer. Cancers (Basel), 16(1), 148.en_US
dc.identifier.doi10.3390/cancers16010148
dc.identifier.endpage19en_US
dc.identifier.issue1en_US
dc.identifier.pmid38201575
dc.identifier.scopus2-s2.0-85182186613
dc.identifier.scopusqualityN/A
dc.identifier.startpage1en_US
dc.identifier.urihttps://www.mdpi.com/2072-6694/16/1/148
dc.identifier.urihttps://hdl.handle.net/11468/13234
dc.identifier.volume16en_US
dc.identifier.wosWOS:001139580500001
dc.identifier.wosqualityN/A
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.institutionauthorVarışli, Lokman
dc.language.isoenen_US
dc.publisherMDPIen_US
dc.relation.ispartofCancers (Basel)
dc.relation.publicationcategoryDiğeren_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectOGG1en_US
dc.subjectNFκBen_US
dc.subjectGene regulationen_US
dc.subjectMicroenvironmenten_US
dc.subjectEMTen_US
dc.subjectInnate immunityen_US
dc.subjectCancer stem cellsen_US
dc.subjectLung canceren_US
dc.subjectAcute myeloid leukemiaen_US
dc.subjectOxidant stressen_US
dc.titleOGG1 as an epigenetic reader affects NF?B: What this means for canceren_US
dc.titleOGG1 as an epigenetic reader affects NF?B: What this means for cancer
dc.typeOtheren_US

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