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Blood, 1 October 2000, Vol. 96, No. 7, pp. 2557-2561
NEOPLASIA
Recruitment of the nuclear receptor corepressor N-CoR by the TEL
moiety of the childhood leukemia-associated TEL-AML1
oncoprotein
Fabien Guidez,
Kevin Petrie,
Anthony M. Ford,
Huafeng Lu,
Caroline A. Bennett,
Angus MacGregor,
Jürgen Hannemann,
Yoshiaki Ito,
Jacques Ghysdael,
Mel Greaves,
Leanne M. Wiedemann, and
Arthur Zelent
From the Leukaemia Research Fund Centre at the
Institute of Cancer Research, Chester Beatty Laboratories, London,
England; the Department of Viral Oncology, Institute of Virus Research,
Kyoto University, Kyoto, Japan; and the CNRS UMR 146, Institut
Curie, Section de Recherche, Centre Universitaire, Orsay, France.
The t(12;21)(p13;q22) chromosomal translocation is the most
frequent illegitimate gene recombination in a pediatric cancer and
occurs in approximately 25% of common acute lymphoblastic leukemia
(cALL) cases. This rearrangement results in the in frame fusion of the
5'-region of the ETS-related gene, TEL
(ETV6), to almost the entire acute myeloid leukemia 1 (AML1) (also called CBFA2 or
PEBP2AB1) locus and expression of the TEL-AML1 chimeric protein. Although AML1 stimulates transcription, TEL-AML1 functions as
a repressor of some AML1 target genes. In contrast to the wild type AML1 protein, both TEL and TEL-AML1 interact with N-CoR, a
component of the nuclear receptor corepressor complex with histone deacetylase activity. The interaction between TEL and N-CoR requires the central region of TEL, which is retained in TEL-AML1, and TEL
lacking this domain is impaired in transcriptional repression. Taken
together, our results suggest that TEL-AML1 may contribute to
leukemogenesis by recruiting N-CoR to AML1 target genes and thus
imposing an altered pattern of their expression.
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