DEK Expression is controlled by E2F and deregulated in diverse tumor types.
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.
Carro
Maria Stella
MS
The FIRC Institute of Molecular Oncology Foundation, Department of Experimental Oncology, European Institute of Oncology, Milan, Italy.
Spiga
Fabio Mario
FM
Quarto
Micaela
M
Di Ninni
Valentina
V
Volorio
Sara
S
Alcalay
Myriam
M
Müller
Heiko
H
D001665:Binding Sites; D002868:Chromosomal Proteins, Non-Histone / Q000235:genetics*; D050684:E2F Transcription Factors / Q000502:physiology*; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D046228:Microarray Analysis; D009369:Neoplasms / Q000378:metabolism / Q000473:pathology*; D015513:Oncogene Proteins / Q000235:genetics*; D000075223:Poly-ADP-Ribose Binding Proteins; D011401:Promoter Regions, Genetic
D002868:Chromosomal Proteins, Non-Histone; C084738:DEK protein, human; D050684:E2F Transcription Factors; D015513:Oncogene Proteins; D000075223:Poly-ADP-Ribose Binding Proteins