Block of granulocytic differentiation of 32Dcl3 cells by AML1/ETO(MTG8) but not by highly expressed Bcl-2

Hidetsugu Kohzaki; Kosei Ito; Gang Huang; Hee Jun Wee; Yota Murakami; Yoshiaki Ito

doi:10.1038/sj.onc.1202735

Block of granulocytic differentiation of 32Dcl3 cells by AML1/ETO(MTG8) but not by highly expressed Bcl-2

Hidetsugu Kohzaki, Kosei Ito, Gang Huang, Hee Jun Wee, Yota Murakami, Yoshiaki Ito

Research output: Contribution to journal › Article › peer-review

37 Scopus citations

Abstract

The chimeric gene, AML1/ETO (MTG8), generated in t(8;21) acute myeloid leukemia enhances the expression of Bcl-2. To evaluate whether this enhancement is the primary role of AML1/ETO in leukemogenesis, effects of over-expression of Bcl-2 in the murine myeloid precursor cell line, 32Dcl3, were examined. When 32Dcl3 cells expressing exogenous Bcl-2 were induced to differentiate, the onset of morphological differentiation was delayed. However, even the cells expressing very high levels of exogenous Bcl-2 eventually underwent differentiation without a significant decrease in the synthesis of Bcl-2. On the contrary, 32Dcl3 cells stably expressing AML1/ETO were completely resistant to differentiation and continued to grow in the presence of G-CSF. These results are consistent with the interpretation that stimulation of Bcl-2 expression is not the primary target of AML1/ETO.

Original language	English (US)
Pages (from-to)	4055-4062
Number of pages	8
Journal	Oncogene
Volume	18
Issue number	28
DOIs	https://doi.org/10.1038/sj.onc.1202735
State	Published - Jul 15 1999
Externally published	Yes

Keywords

32Dcl3
AML1
AML1/ETO(MTG8)
Bcl-2
Granulocytic differentiation

ASJC Scopus subject areas

Genetics
Molecular Biology
Cancer Research

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10.1038/sj.onc.1202735

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title = "Block of granulocytic differentiation of 32Dcl3 cells by AML1/ETO(MTG8) but not by highly expressed Bcl-2",

abstract = "The chimeric gene, AML1/ETO (MTG8), generated in t(8;21) acute myeloid leukemia enhances the expression of Bcl-2. To evaluate whether this enhancement is the primary role of AML1/ETO in leukemogenesis, effects of over-expression of Bcl-2 in the murine myeloid precursor cell line, 32Dcl3, were examined. When 32Dcl3 cells expressing exogenous Bcl-2 were induced to differentiate, the onset of morphological differentiation was delayed. However, even the cells expressing very high levels of exogenous Bcl-2 eventually underwent differentiation without a significant decrease in the synthesis of Bcl-2. On the contrary, 32Dcl3 cells stably expressing AML1/ETO were completely resistant to differentiation and continued to grow in the presence of G-CSF. These results are consistent with the interpretation that stimulation of Bcl-2 expression is not the primary target of AML1/ETO.",

keywords = "32Dcl3, AML1, AML1/ETO(MTG8), Bcl-2, Granulocytic differentiation",

author = "Hidetsugu Kohzaki and Kosei Ito and Gang Huang and Wee, {Hee Jun} and Yota Murakami and Yoshiaki Ito",

note = "Funding Information: We thank M Tsujimoto (Osaka University), H Yamauchi and S Fujita (Ehime University), A Friedman (Johns Hopkins University) and T Era (Osaka University) for Bcl-2 cDNA (pSKMBKR), ME-1 cells, 32Dcl3 cells and AML1/ETO cDNA, respectively. This work was supported by Grant-in-Aid 0925322 for Priority Area on Cancer Research from the Ministry of Education, Science and Culture, Japan.",

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T1 - Block of granulocytic differentiation of 32Dcl3 cells by AML1/ETO(MTG8) but not by highly expressed Bcl-2

AU - Kohzaki, Hidetsugu

AU - Ito, Kosei

AU - Huang, Gang

AU - Wee, Hee Jun

AU - Murakami, Yota

AU - Ito, Yoshiaki

N1 - Funding Information: We thank M Tsujimoto (Osaka University), H Yamauchi and S Fujita (Ehime University), A Friedman (Johns Hopkins University) and T Era (Osaka University) for Bcl-2 cDNA (pSKMBKR), ME-1 cells, 32Dcl3 cells and AML1/ETO cDNA, respectively. This work was supported by Grant-in-Aid 0925322 for Priority Area on Cancer Research from the Ministry of Education, Science and Culture, Japan.

PY - 1999/7/15

Y1 - 1999/7/15

N2 - The chimeric gene, AML1/ETO (MTG8), generated in t(8;21) acute myeloid leukemia enhances the expression of Bcl-2. To evaluate whether this enhancement is the primary role of AML1/ETO in leukemogenesis, effects of over-expression of Bcl-2 in the murine myeloid precursor cell line, 32Dcl3, were examined. When 32Dcl3 cells expressing exogenous Bcl-2 were induced to differentiate, the onset of morphological differentiation was delayed. However, even the cells expressing very high levels of exogenous Bcl-2 eventually underwent differentiation without a significant decrease in the synthesis of Bcl-2. On the contrary, 32Dcl3 cells stably expressing AML1/ETO were completely resistant to differentiation and continued to grow in the presence of G-CSF. These results are consistent with the interpretation that stimulation of Bcl-2 expression is not the primary target of AML1/ETO.

AB - The chimeric gene, AML1/ETO (MTG8), generated in t(8;21) acute myeloid leukemia enhances the expression of Bcl-2. To evaluate whether this enhancement is the primary role of AML1/ETO in leukemogenesis, effects of over-expression of Bcl-2 in the murine myeloid precursor cell line, 32Dcl3, were examined. When 32Dcl3 cells expressing exogenous Bcl-2 were induced to differentiate, the onset of morphological differentiation was delayed. However, even the cells expressing very high levels of exogenous Bcl-2 eventually underwent differentiation without a significant decrease in the synthesis of Bcl-2. On the contrary, 32Dcl3 cells stably expressing AML1/ETO were completely resistant to differentiation and continued to grow in the presence of G-CSF. These results are consistent with the interpretation that stimulation of Bcl-2 expression is not the primary target of AML1/ETO.

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Block of granulocytic differentiation of 32Dcl3 cells by AML1/ETO(MTG8) but not by highly expressed Bcl-2

Abstract

Keywords

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