Cell fate of hematopoietic progenitors is regulated by interaction between
Notch proteins on progenitors and Notch ligands such as Jagged1 on stromal
cells. Since acute myeloid leukemia (AML) originates from dysregulated hema
topoietic progenitors, some abnormalities in the Notch-Jagged system may ex
ist in AML cells. As the first step to clarify this, we examined the expres
sion of Notch1 and Jagged1 proteins in eight AML cell lines and 15 fresh AM
L samples by immunoblotting. In the Notch1 protein, two bands, a 300 kDa ba
nd and a 120 kDa band, which appeared to be a full-length protein and a tra
nsmembrane fragment, respectively, were recognized in five AML cell lines a
nd six fresh samples. In addition, three of the five cell lines showed a 11
0 kDa fragment, which appeared to be from an intracellular domain, namely a
n active form. One cell line showed aberrant sized fragments, which suggest
ed a structural abnormality. Jagged1 protein was recognized in six cell lin
es and six fresh samples. In four cell lines and four fresh samples, both N
otch1 and Jagged1 proteins were observed. In these cells, Notch1 and Jagged
1 proteins may interact among themselves. We showed that Notch1 and Jagged1
proteins are widely expressed in AML. cells. We hypothesize that some abno
rmalities in the Notch-Jagged system which cause the excessive self-renewal
and the block of differentiation, may be involved in the abnormal prolifer
ation of AML cells.