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Blood, 15 April 2001, Vol. 97, No. 8, pp. 2449-2456
NEOPLASIA
Myeloblastin is an Myb target gene: mechanisms of regulation in
myeloid leukemia cells growth-arrested by retinoic acid
Pierre G. Lutz,
Anne Houzel-Charavel,
Christel Moog-Lutz, and
Yvon E. Cayre
From Unité INSERM U417, Hôpital Saint
Antoine, Paris, France; and Department of Microbiology/Immunology,
Kimmel Cancer Institute, Thomas Jefferson University, Philadelphia, PA.
A pivotal role has been assigned to Myb in the control of
myeloid cell growth. Although Myb is a target of retinoic acid, little
is known about the mechanisms by which it may contribute to induced
growth arrest in leukemia cells. Indeed, few Myb target genes are known
to be linked to proliferation. Myeloblastin is involved in the control
of proliferation in myeloid leukemia cells. It is expressed early
during hematopoiesis and is a granulocyte colony-stimulating
factor-responsive gene. Myeloblastin can confer factor-independent
growth to hematopoietic cells, an early step in leukemia
transformation. The myeloblastin promoter contains PU.1, C/EBP, and Myb
binding sites, each of which are critical for constitutive expression
in myeloid cells. Inhibition of myeloblastin expression in
leukemia cells growth-arrested by retinoic acid is demonstrated to
depend on Myb down-regulation. Myb is shown to induce myeloblastin
expression and abolish its down-regulation by retinoic acid.
Altogether, the data offer a clue as to how a myeloid-specific
transcriptional machinery can be accessible to regulation by retinoic
acid and point to myeloblastin as a novel target of Myb. This link
between Myb and myeloblastin suggests a previously nonidentified Myb
pathway through which growth arrest is induced by retinoic acid in
myeloid leukemia cells.
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