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Blood, Vol. 96 No. 1 (July 1), 2000:
pp. 288-296
AML1-MTG8 leukemic protein induces the expression of
granulocyte colony-stimulating factor (G-CSF) receptor through the
up-regulation of CCAAT/enhancer binding protein epsilon
Kimiko Shimizu,
Issay Kitabayashi,
Nanao Kamada,
Tatsuo Abe,
Nobuo Maseki,
Kazumi Suzukawa, and
Misao Ohki
From the Radiobiology Division, National Cancer Center Research
Institute, Tsukiji, Chuo-ku, Tokyo 104-0045, Japan.
The t(8;21) translocation is one of the most frequent chromosomal
abnormalities associated with acute myeloid leukemia (AML). In this
translocation, the AML1 (CBFA2/PEBP2aB) gene is
disrupted and fused to the MTG8 (ETO) gene. The ectopic
expression of the resulting AML1-MTG8 fusion gene product in
L-G and 32Dcl3 murine myeloid precursor cells stimulates cell
proliferation without inducing morphologic terminal differentiation
into mature granulocytes in response to granulocyte-colony stimulating
factor (G-CSF). This study found that the ectopic expression of
AML1-MTG8 elevates the expression of the G-CSF receptor (G-CSFR).
Analysis of the promoter region of the G-CSFR gene revealed
that up-regulation of G-CSFR expression by AML1-MTG8 does not depend on
the AML1-binding sequence, but on the C/EBP (CCAAT/enhancer binding
protein) binding site. The results suggest that the overproduction of
G-CSFR is at least partly mediated by C/EBP , whose expression is
activated by AML1-MTG8. The ectopic expression of G-CSFR in L-G cells
induced cell proliferation in response to G-CSF, but did not inhibit
cell differentiation into mature neutrophils. Overexpression of
C/EBP in L-G cells also stimulated G-CSF-dependent cell
proliferation. High expression levels of G-CSFR were also found in the
leukemic cells of AML patients with t(8;21). Therefore,
G-CSF-dependent cell proliferation of myeloid precursor cells may be
implicated in leukemogenesis.
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