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

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      Author(s)
      Özçelik, Emrah
      Kalaycı, Ahmet
      Çelik, Büşra
      Avcı, Açelya
      Akyol, Hasan
      Kılıç, İrfan Baki
      Güzel, Türkan
      Çetin, Metin
      Öztürk, Merve Tuzlakoğlu
      Çalışkaner, Zihni Onur
      Tombaz, Melike
      Yoleri, Dilan
      Konu, Özlen
      Kandilci, Ayten
      Date
      2022-10-03
      Source Title
      PLoS ONE
      Print ISSN
      19326203
      Publisher
      Public Library of Science
      Volume
      17
      Issue
      10
      Pages
      1 - 19
      Language
      English
      Type
      Article
      Item Usage Stats
      3
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      Abstract
      DEK 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.
      Keywords
      Amino Acids
      Chromosomal Proteins
      Non-Histone
      DNA Damage
      Doxorubicin
      Humans
      Oncogene Proteins
      Poly-ADP-Ribose Binding Proteins
      Protein Isoforms
      RNA
      Small Interfering
      Permalink
      http://hdl.handle.net/11693/111998
      Published Version (Please cite this version)
      https://dx.doi.org/10.1371/journal.pone.0275476
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