Truncated AML1 proteins are predicted to be expressed from out-of-frame AML1 transcripts present in myeloid leukemia cells harboring t(8;21) and t(3;21). To test whether these pro teins, consisting of almost exclusively an N-terminal AML1 DNA-binding domain, interfere with myeloid differentiation we expressed a similar trunctated AML1 protein in 32D cl3 myeloid cells. In all clones examined, the ectopically expressed truncated AML1 protein prevented binding of endogenous PEBP2/CBFs to DNA, possibly by interacting with all available CBFβ subunits. However, compared to control clones, the 32D cl3 clones expressing truncated AML1 remained IL-3 dependent for survival, proliferated similarly in low and high concentrations of IL-3, and differentiated similarly upon transfer to GCSF. Thus, truncated AML1 proteins may contribute to myeloid leukemogenesis by inhibiting PEBP2/CBF activities, although contributions from other oncoproteins are likely required as well.
|Original language||English (US)|
|Number of pages||7|
|State||Published - Jun 1996|
ASJC Scopus subject areas
- Cancer Research