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Blood, Vol. 96 No. 2 (July 15), 2000:
pp. 655-663
Analysis of genes under the downstream control of the t(8;21)
fusion protein AML1-MTG8: overexpression of the TIS11b
(ERF-1, cMG1) gene induces myeloid cell
proliferation in response to G-CSF
Hiroyuki Shimada,
Hitoshi Ichikawa,
Sawako Nakamura,
Rieko Katsu,
Mitsuteru Iwasa,
Issay Kitabayashi, and
Misao Ohki
From the Cancer Genomics Division, National Cancer
Center Research Institute, Tokyo, Japan.
The AML1-MTG8 fusion transcription factor generated by t(8;21)
translocation is thought to dysregulate genes that are crucial for
normal differentiation and proliferation of hematopoietic progenitors
to cause acute myelogenous leukemia (AML). Although AML1-MTG8 has been
shown to repress the transcription of AML1 targets, none of the known
targets of AML1 are probably responsible for AML1-MTG8-mediated
leukemogenesis. In this study, 24 genes under the downstream control of
AML1-MTG8 were isolated by using a differential display technique.
Analysis with deletion mutants of AML1-MTG8 demonstrated that the
regulation of the majority of these genes requires the region of 51 residues (488-538) containing the Nervy homology region 2 (NHR2),
through which AML1-MTG8 interacts with MTGR1. Among the 24 genes
identified, 10 were considered to be genes under the control of AML1,
because their expression was altered by AML1b or AML1a or both.
However, the other 14 genes were not affected by either AML1b or AML1a,
suggesting the possibility that AML1-MTG8 regulates a number of
specific target genes that are not normally regulated by AML1.
Furthermore, an up-regulated gene, TIS11b (ERF-1,
cMG1), was highly expressed in t(8;21) leukemic cells, and the
overexpression of TIS11b induced myeloid cell proliferation in
response to granulocyte colony-stimulating factor. These results suggest that the high-level expression of TIS11b contributes to AML1-MTG8-mediated leukemogenesis.
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