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The shortest isoform of C/EBPβ, liver inhibitory protein (LIP), collaborates with Evi1 to induce AML in a mouse BMT model.

Abstract：

:Ecotropic viral integration site 1 (Evi1) is one of the master regulators in the development of acute myeloid leukemia (AML) and myelodysplastic syndrome. High expression of Evi1 is found in 10% of patients with AML and indicates a poor outcome. Several recent studies have indicated that Evi1 requires collaborative factors to induce AML. Therefore, the search for candidate factors that collaborate with Evi1 in leukemogenesis is one of the key issues in uncovering the mechanism of Evi1-related leukemia. Previously, we succeeded in making a mouse model of Evi1-related leukemia using a bone marrow transplantation (BMT) system. In the Evi1-induced leukemic cells, we identified frequent retroviral integrations near the CCAAT/enhancer-binding protein β (C/EBPβ) gene and overexpression of its protein. These findings imply that C/EBPβ is a candidate gene that collaborates with Evi1 in leukemogenesis. Cotransduction of Evi1 and the shortest isoform of C/EBPβ, liver inhibitory protein (LIP), induced AML with short latencies in a mouse BMT model. Overexpression of LIP alone also induced AML with longer latencies. However, excision of all 3 isoforms of C/EBPβ (LAP*/LAP/LIP) did not inhibit the development of Evi1-induced leukemia. Therefore, isoform-specific intervention that targets LIP is required when we consider C/EBPβ as a therapeutic target.

journal_name

Blood

journal_title

Blood

authors

Watanabe-Okochi N,Yoshimi A,Sato T,Ikeda T,Kumano K,Taoka K,Satoh Y,Shinohara A,Tsuruta T,Masuda A,Yokota H,Yatomi Y,Takahashi K,Kitaura J,Kitamura T,Kurokawa M

doi

10.1182/blood-2011-07-368654

subject

Has Abstract

pub_date

2013-05-16 00:00:00

pages

4142-55

issue

20

eissn

0006-4971

issn

1528-0020

pii

blood-2011-07-368654

journal_volume

121

pub_type

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