DEK protein level is a biomarker of CD138positive normal and malignant plasma cells

dc.contributor.authorCaliskaner, Zihni Onur
dc.contributor.authorCakar, Turkan
dc.contributor.authorOzcelik, Emrah
dc.contributor.authorOzdilik, Ahmet
dc.contributor.authorKim, Annette S.
dc.contributor.authorDogan, Oner
dc.contributor.authorBosompem, Amma
dc.date.accessioned2025-10-29T11:12:25Z
dc.date.issued2017
dc.departmentFakülteler, Temel Bilimler Fakültesi, Moleküler Biyoloji ve Genetik Bölümü
dc.description.abstractOverexpression of DEK oncogene is associated with increased proliferation of carcinoma cells and it is observed in several solid tumors due to the amplification of the 6p22.3 chromosomal region where DEK locates. Although the same chromosomal amplification occurs in multiple myeloma (MM), a plasma cell neoplasm, whether the expression and the copy number of the DEK gene are affected in MM remains elusive. We show that despite the increased copy number in CD138(positive) MM cells (4 out of 41 MM samples), DEK mRNA expression was down-regulated compared with that in CD138(negative) bone marrow (BM) cells of the same patients (P< 0.0001). DEK protein was not detectable by immunohistochemistry (IHC) in CD138(positive) normal plasma cells or in malignant plasma cells of MM patients (n = 56) whereas it was widely expressed in normal and neoplastic B-cells. Stable knockdown or overexpression of DEK in CD138(positive) MM cell lines did not affect the proliferation and viability of the cells profoundly in the presence or absence of chemotherapeutic agent melphalan whereas knockdown of DEK moderately but significantly increased the expression level of CD138 (p< 0.01). Decreased DEK expression in plasma cells suggests a potential role of this gene in plasma cell development and lack of detectable DEK protein by IHC could be used as a biomarker for normal and malignant plasma cells.
dc.description.sponsorshipScientific and Technological Research Council of Turkey (TUEBITAK) [KBAG212T108]
dc.description.sponsorshipGebze Technical University Research Fund [BAP-2015-A14]
dc.description.sponsorshipNCI/NIH Cancer Center [2P30CA06848514]
dc.description.sponsorshipThis work was supported by the Scientific and Technological Research Council of Turkey (TUEBITAK) Grant (KBAG212T108) and Gebze Technical University Research Fund (BAP-2015-A14). Samples were obtained from the Translational Pathology Shared Resource at Vanderbilt University Medical Center that is supported by NCI/NIH Cancer Center Support Grant 2P30CA06848514.
dc.identifier.doi10.1371/journal.pone.0178025
dc.identifier.issn1932-6203
dc.identifier.issue5
dc.identifier.orcid0000-0003-1385-1739
dc.identifier.pmid28558048
dc.identifier.urihttps://doi.org/10.1371/journal.pone.0178025
dc.identifier.urihttps://hdl.handle.net/20.500.14854/6264
dc.identifier.volume12
dc.identifier.wosWOS:000402607000022
dc.identifier.wosqualityQ1
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherPublic Library Science
dc.relation.ispartofPlos One
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/openAccess
dc.snmzKA_WOS_20251020
dc.subjectMultiple-Myeloma
dc.subjectOverexpression
dc.subjectExpression
dc.subjectGene
dc.subjectProtooncogene
dc.subjectInhibitor
dc.titleDEK protein level is a biomarker of CD138positive normal and malignant plasma cells
dc.typeArticle

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