Doxorubicin induces prolonged DNA damage signal in cells overexpressing DEK isoform-2

buir.contributor.authorTombaz, Melike
buir.contributor.authorKonu, Özlen
buir.contributor.orcidTombaz, Melike|0000-0002-0528-6680
buir.contributor.orcidKonu, Özlen|0000-0002-6223-5329
dc.citation.epage19en_US
dc.citation.issueNumber10en_US
dc.citation.spage1en_US
dc.citation.volumeNumber17en_US
dc.contributor.authorÖzçelik, Emrah
dc.contributor.authorKalaycı, Ahmet
dc.contributor.authorÇelik, Büşra
dc.contributor.authorAvcı, Açelya
dc.contributor.authorAkyol, Hasan
dc.contributor.authorKılıç, İrfan Baki
dc.contributor.authorGüzel, Türkan
dc.contributor.authorÇetin, Metin
dc.contributor.authorÖztürk, Merve Tuzlakoğlu
dc.contributor.authorÇalışkaner, Zihni Onur
dc.contributor.authorTombaz, Melike
dc.contributor.authorYoleri, Dilan
dc.contributor.authorKonu, Özlen
dc.contributor.authorKandilci, Ayten
dc.date.accessioned2023-03-01T11:51:18Z
dc.date.available2023-03-01T11:51:18Z
dc.date.issued2022-10-03
dc.departmentDepartment of Molecular Biology and Geneticsen_US
dc.description.abstractDEK has a short isoform (DEK isoform-2; DEK2) that lacks amino acid residues between 49–82. The full-length DEK (DEK isoform-1; DEK1) is ubiquitously expressed and plays a role in different cellular processes but whether DEK2 is involved in these processes remains elusive. We stably overexpressed DEK2 in human bone marrow stromal cell line HS-27A, in which endogenous DEKs were intact or suppressed via short hairpin RNA (sh-RNA). We have found that contrary to ectopic DEK1, DEK2 locates in the nucleus and nucleolus, causes persistent үH2AX signal upon doxorubicin treatment, and couldn’t functionally compensate for the loss of DEK1. In addition, DEK2 overexpressing cells were more sensitive to doxorubicin than DEK1-cells. Expressions of DEK1 and DEK2 in cell lines and primary tumors exhibit tissue specificity. DEK1 is upregulated in cancers of the colon, liver, and lung compared to normal tissues while both DEK1 and DEK2 are downregulated in subsets of kidney, prostate, and thyroid carcinomas. Interestingly, only DEK2 was downregulated in a subset of breast tumors suggesting that DEK2 can be modulated differently than DEK1 in specific cancers. In summary, our findings show distinct expression patterns and subcellular location and suggest non-overlapping functions between the two DEK isoforms. © 2022 Ozçelik et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.en_US
dc.description.provenanceSubmitted by Cem Çağatay Akgün (cem.akgun@bilkent.edu.tr) on 2023-03-01T11:51:18Z No. of bitstreams: 1 Doxorubicin_induces_prolonged_DNA_damage_signal_in_cells_overexpressing_DEK_isoform-2.pdf: 3654287 bytes, checksum: 07a7430bc0584433f24585a44b7e6f69 (MD5)en
dc.description.provenanceMade available in DSpace on 2023-03-01T11:51:18Z (GMT). No. of bitstreams: 1 Doxorubicin_induces_prolonged_DNA_damage_signal_in_cells_overexpressing_DEK_isoform-2.pdf: 3654287 bytes, checksum: 07a7430bc0584433f24585a44b7e6f69 (MD5) Previous issue date: 2022-10-03en
dc.identifier.doi10.1371/journal.pone.0275476en_US
dc.identifier.issn19326203
dc.identifier.urihttp://hdl.handle.net/11693/111998
dc.language.isoEnglishen_US
dc.publisherPublic Library of Scienceen_US
dc.relation.isversionofhttps://dx.doi.org/10.1371/journal.pone.0275476en_US
dc.source.titlePLoS ONEen_US
dc.subjectAmino Acidsen_US
dc.subjectChromosomal Proteinsen_US
dc.subjectNon-Histoneen_US
dc.subjectDNA Damageen_US
dc.subjectDoxorubicinen_US
dc.subjectHumansen_US
dc.subjectOncogene Proteinsen_US
dc.subjectPoly-ADP-Ribose Binding Proteinsen_US
dc.subjectProtein Isoformsen_US
dc.subjectRNAen_US
dc.subjectSmall Interferingen_US
dc.titleDoxorubicin induces prolonged DNA damage signal in cells overexpressing DEK isoform-2en_US
dc.typeArticleen_US

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