ABSTRACT AML1-ETO, a leukemia-associated fusion protein generated by the frequently occurred chromosome translocation t(8;21) in acute myeloid leukemia, was shown to exert dichotomous

functions in leukemic cells, that is, growth arrest versus differentiation block. By the analysis of oligonucleotide microarray, AML1-ETO was shown to modulate the expressions of an

impressive array of pro- and anti-apoptotic genes. Here, we investigate potential effects of the ecdysone inducible AML1-ETO expression on apoptosis of leukemic U937 cell line. We show that

AML1-ETO significantly stabilizes death receptor Fas protein and increases proapoptotic Bak in addition to reducing Bcl-2 expression. Accordingly, inducible AML1-ETO expression is followed

it must be overcome to fulfill their leukemogenic potential. Complementary to this prediction is that two AML1-ETO-carrying leukemic cells, Kasumi-1 and SKNO-1, present similar sensitivity

to apoptosis induction with AML1-ETO-negative leukemic cells. Therefore, genetic and/or epigenetic screenings of apoptosis-related genes modulated by AML1-ETO deserve to be explored for

understanding the mechanisms of AML1-ETO-induced leukemogenesis. Access through your institution Buy or subscribe This is a preview of subscription content, access via your institution

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MYELOID LEUKEMIA Article Open access 20 December 2021 ABL1 KINASE AS A TUMOR SUPPRESSOR IN AML1-ETO AND NUP98-PMX1 LEUKEMIAS Article Open access 23 March 2023 CUT-LIKE HOMEOBOX 1 (_CUX1_)

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hematopoietic cells. _Leukemia_ 2005; 19: 1794–1805. Article  CAS  PubMed  Google Scholar  Download references ACKNOWLEDGEMENTS We thank Dr Zhu YS in Weill Medical College of Cornell

University, New York for his careful editing assistance. We also deeply appreciate two anonymous reviewers for their thoughtful and serious evaluations on this work. Mrs Lu Y is a PhD

candidate at Shanghai Jiaotong University School of Medicine, and this work is submitted in partial fulfillment of the requirement for her PhD. This work was supported in part by National

Key Program (973) for Basic Research of China (NO2002CB512805) and National Natural Science Foundation of China (90408009 and 30500257). Grants from Science and Technology Committee of

Shanghai (03XD14016, 05JC14032) should also be acknowledged. AUTHOR INFORMATION AUTHORS AND AFFILIATIONS * The Department of Pathophysiology, Key Laboratory of Cell Differentiation and

Apoptosis of Chinese Ministry of Education, Rui-Jin Hospital, Shanghai Jiao-Tong University School of Medicine, Shanghai, China Y Lu, Y-B Xu & G-Q Chen * Institute of Health Science,

Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, China T-T Yuan, M-G Song & G-Q Chen * The Department of Medicine, University of Freiburg Medical

Center, Freiburg, Germany M Lübbert & M Fliegauf Authors * Y Lu View author publications You can also search for this author inPubMed Google Scholar * Y-B Xu View author publications You

can also search for this author inPubMed Google Scholar * T-T Yuan View author publications You can also search for this author inPubMed Google Scholar * M-G Song View author publications

You can also search for this author inPubMed Google Scholar * M Lübbert View author publications You can also search for this author inPubMed Google Scholar * M Fliegauf View author

publications You can also search for this author inPubMed Google Scholar * G-Q Chen View author publications You can also search for this author inPubMed Google Scholar CORRESPONDING AUTHOR

Correspondence to G-Q Chen. RIGHTS AND PERMISSIONS Reprints and permissions ABOUT THIS ARTICLE CITE THIS ARTICLE Lu, Y., Xu, YB., Yuan, TT. _et al._ Inducible expression of AML1-ETO fusion

protein endows leukemic cells with susceptibility to extrinsic and intrinsic apoptosis. _Leukemia_ 20, 987–993 (2006). https://doi.org/10.1038/sj.leu.2404218 Download citation * Received: 28

November 2005 * Revised: 23 February 2006 * Accepted: 02 March 2006 * Published: 06 April 2006 * Issue Date: 01 June 2006 * DOI: https://doi.org/10.1038/sj.leu.2404218 SHARE THIS ARTICLE

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by the Springer Nature SharedIt content-sharing initiative KEYWORDS * AML1-ETO * apoptosis * Fas * Bak