DEK expression is controlled by E2F and deregulated in diverse tumor types

Maria Stella Carro, Fabio Mario Spiga, Micaela Quarto, Valentina Di Ninni, Sara Volorio, Myriam Alcalay, Heiko Müller

Research output: Contribution to journalArticlepeer-review


Deregulation of the retinoblastoma (pRB) tumor suppressor pathway associated with aberrant activity of E2F transcription factors is frequently observed in human cancer. Microarray based analyses have revealed a large number of potential downstream mediators of the tumor suppressing activity of pRB, including DEK, a fusion partner of CAN found in a subset of acute myeloid leukaemia (AML) patients carrying a (6; 9) translocation. Here we report that the expression of DEK is under direct control of E2F transcription factors. Chromatin immunoprecipitation assays show that the DEK promoter is bound by endogenous E2F in vivo. The DEK promoter is transactivated by E2F and mutation of E2F binding sites eliminates this effect. Expression levels of DEK in human tumors have been investigated by tissue micro array analysis. We find that DEK is overexpressed in many solid tumors such as colon cancer, larynx cancer, bladder cancer, and melanoma.

Original languageEnglish
Pages (from-to)1202-1207
Number of pages6
JournalCell Cycle
Issue number11
Publication statusPublished - Jun 1 2006


  • Cancer
  • DEK
  • E2F
  • Overexpression
  • Tissue microarray

ASJC Scopus subject areas

  • Cell Biology
  • Biochemistry
  • Molecular Biology


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