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EWS-ATF-1 chimeric protein in soft tissue clear cell sarcoma associates with CREB-binding protein and interferes with p53- mediated trans-activation function

  1. Author:
    Fujimura, Y.
    Siddique, H.
    Lee, L.
    Rao, V. N.
    Reddy, E. S. P.

  2. Author Address

    Med Coll Penn & Hahnemann Univ, Sch Med, Program Canc Genet, Canc Ctr, Dept Biochem, Broad & Vine, MS 481, Philadelphia, PA 19102 USA. Med Coll Penn & Hahnemann Univ, Sch Med, Program Canc Genet, Canc Ctr, Dept Biochem, Philadelphia, PA 19102 USA. SAIC, Frederick, MD 21702 USA. Reddy ESP Med Coll Penn & Hahnemann Univ, Sch Med, Program Canc Genet, Canc Ctr, Dept Biochem, Broad & Vine, MS 481, Philadelphia, PA 19102 USA.
    1. Year: 2001
  2. Journal: Oncogene
    1. 20
    2. 46
    3. Pages: 6653-6659
  4. Type of Article: Article
  1. Abstract:

    The recurrent t(12;22) (q13;q12) chromosomal translocation associated with soft tissue clear cell sarcoma results in a chimeric protein EWS-ATF-1 that acts as a constitutive transcriptional activator. The CBP/p300 transcriptional coactivator, which links various transcriptional factors to basal transcription apparatus, participates in transcriptional activation, growth and cell cycle control and differentiation. In this study, we show that EWS-ATF-1 associates constitutively with CBP both in vitro and in vivo. Both EWS and ATF-1 fusion domains are needed for this interaction. Here, we demonstrate that EWS-ATF-1 represses p53/CBP-mediated transactivation function. Overexpression of CBP can counteract this repressive effect of EWS-ATF-1. Taken together, these findings suggest that one of the mechanisms by which EWS-ATF-1 may cause tumors is through targeting CBP/p300 resulting in the loss of function of p53. This novel mechanism may be responsible for the development of these and other related solid tumors.

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