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Blood, 1 May 2001, Vol. 97, No. 9, pp. 2784-2790
NEOPLASIA
Cytokine-regulated expression of survivin
in myeloid leukemia
Bing Z. Carter,
Michele Milella,
Dario C. Altieri, and
Michael Andreeff
From the University of Texas M. D. Anderson Cancer
Center, Houston, TX; the Division of Medical Oncology I, Regina Elena
Cancer Institute, Rome, Italy; and Yale University School of Medicine,
New Haven, CT.
Survivin, a member of the inhibitors-of-apoptosis gene
family, is expressed in a cell-cycle-dependent manner in all the most common cancers but not in normal differentiated adult tissues. Survivin expression and regulation were examined in acute
myeloid leukemia (AML). Survivin was detected by Western
blot analysis in all myeloid leukemia cell lines and in 16 of 18 primary AML samples tested. In contrast, normal CD34+ cells
and normal peripheral blood mononuclear cells expressed no or very low
levels of survivin. Cytokine stimulation increased survivin expression in leukemic cell lines and in primary
AML samples. In cultured primary samples, single-cytokine stimulation substantially increased survivin expression in comparison
with control cells, and the combination of G-CSF, GM-CSF, and SCF
increased survivin levels even further. Conversely,
all-trans retinoic acid significantly decreased survivin
protein levels in HL-60, OCI-AML3, and NB-4 cells within 96 hours,
parallel to the induction of myelomonocytic differentiation. Using
selective pharmacologic inhibitors, the differential involvement of
mitogen-activated protein kinase kinase (MEK) and
phosphatidylinositol-3 kinase (PI3K) pathways were demonstrated in the
regulation of survivin expression. The MEK inhibitor
PD98059 down-regulated survivin expression in both resting
and GM-CSF-stimulated OCI-AML3 cells, whereas the PI3K inhibitor
LY294002 inhibited survivin expression only on GM-CSF
stimulation. In conclusion, these results demonstrate that
survivin is highly expressed and cytokine-regulated in
myeloid leukemias and suggest that hematopoietic cytokines exert their
antiapoptotic and mitogenic effects, at least in part, by
increasing survivin levels.
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