ATAD2 is a novel cofactor for MYC, overexpressed and amplified in aggressive tumors

Marco Ciró, Elena Prosperini, Micaela Quarto, Ursula Grazini, Julian Walfridsson, Fraser McBlane, Paolo Nucifero, Giovanni Pacchiana, Maria Capra, Jesper Christensen, Kristian Helin

Research output: Contribution to journalArticlepeer-review


The E2F and MYC transcription factors are critical regulators of cell proliferation and contribute to the development of human cancers. Here, we report on the identification of a novel E2F target gene, ATAD2, the predicted protein product of which contains both a bromodomain and an ATPase domain. The pRB-E2F pathway regulates ATAD2 expression, which is limiting for the entry into the S phase of the cell cycle. We show that ATAD2 binds the MYC oncogene and stimulates its transcriptional activity. ATAD2 maps to chromosome 8q24, 4.3 Mb distal to MYC, in a region that is frequently found amplified in cancer. Consistent with this, we show that ATAD2 expression is high in several human tumors and that the expression levels correlate with clinical outcome of breast cancer patients. We suggest that ATAD2 links the E2F and MYC pathways and contributes to the development of aggressive cancer through the enhancement of MYC-dependent transcription.

Original languageEnglish
Pages (from-to)8491-8498
Number of pages8
JournalCancer Research
Issue number21
Publication statusPublished - Nov 1 2009

ASJC Scopus subject areas

  • Cancer Research
  • Oncology


Dive into the research topics of 'ATAD2 is a novel cofactor for MYC, overexpressed and amplified in aggressive tumors'. Together they form a unique fingerprint.

Cite this