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

Maria Stella Carro1, Fabio Mario Spiga, Micaela Quarto

  • 1The FIRC Institute of Molecular Oncology Foundation, Department of Experimental Oncology, European Institute of Oncology, Milan, Italy.

Cell Cycle (Georgetown, Tex.)
|May 25, 2006
PubMed

Insights

The retinoblastoma pathway is often deregulated in cancer. This study found that the DEK gene, implicated in certain leukemias, is directly controlled by E2F transcription factors and overexpressed in various solid tumors.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Genetics

Background:

  • Deregulation of the retinoblastoma (pRB) tumor suppressor pathway and aberrant E2F transcription factor activity are common in human cancers.
  • Microarray analyses identified numerous potential downstream mediators of pRB tumor suppression, including the DEK gene.
  • DEK is a fusion partner of CAN in acute myeloid leukemia (AML) with a (6; 9) translocation.

Purpose of the Study:

  • To investigate the regulatory relationship between E2F transcription factors and the DEK gene.
  • To determine if DEK expression is directly controlled by E2F.
  • To analyze DEK expression levels in various human solid tumors.

Main Methods:

  • Chromatin immunoprecipitation (ChIP) assays to detect E2F binding to the DEK promoter in vivo.
  • Reporter assays to assess E2F-mediated transactivation of the DEK promoter.
  • Site-directed mutagenesis to identify functional E2F binding sites.
  • Tissue microarray analysis to quantify DEK expression in human tumors.

Main Results:

  • Endogenous E2F directly binds to the DEK promoter in vivo.
  • E2F transactivates the DEK promoter.
  • Mutation of E2F binding sites abolishes DEK promoter transactivation.
  • DEK is overexpressed in a significant proportion of investigated solid tumors, including colon cancer, larynx cancer, bladder cancer, and melanoma.

Conclusions:

  • DEK expression is directly regulated by E2F transcription factors.
  • The DEK gene is a novel downstream target of the E2F pathway.
  • Overexpression of DEK in various solid tumors suggests its potential role in tumorigenesis and warrants further investigation.

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