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Blood, 15 October 2002, Vol. 100, No. 8, pp. 2917-2925
NEOPLASIA
Induction of apoptosis of human B-CLL and ALL cells by a novel
retinoid and its nonretinoidal analog
Yuxiang Zhang,
Marcia I. Dawson,
Ramzi Mohammad,
Arun K. Rishi,
Lulu Farhana,
Kai-Chia Feng,
Mark Leid,
Valerie Peterson,
Xiao-kun Zhang,
Mark Edelstein,
David Eilander,
Sandra Biggar,
Nathan Wall,
Uwe Reichert, and
Joseph A. Fontana
From the Department of Medicine, Karmanos Cancer
Institute, Wayne State University, and the John D Dingell VA Medical
Center, Detroit, MI; the Burnham Institute, La Jolla, CA; College of
Pharmacy, Oregon State University, Corvallis; and Galderma R and D,
Sophia Antipolis, France.
We have recently described a novel retinoid
6-[3-(1-adamantyl)-4-hydroxyphenyl]-2-naphthalenecarboxylic acid
(CD437/AHPN) that induces apoptosis in a number of malignant cell
types. We now describe our studies examining the effects of CD437 and a nonretinoidal analog (MM002) on the in vitro proliferation of the
ALL-REH cell line, the in vitro and in vivo growth of a novel Epstein-Barr virus-negative (EBV ) B-cell
chronic lymphocytic leukemia (B-CLL) cell line (WSU-CLL), and
primary cultures of human B-CLL and acute lymphoblastic leukemia (ALL) cells. CD437 and MM002 induce apoptosis in both cell
lines, as indicated by the activation of caspase-2 and
caspase-3, cleavage of poly(adenosine diphosphate-ribose)
(poly(ADP-ribose)) polymerase, increase in annexin V binding,
and subsequent nuclear fragmentation. CD437-mediated apoptosis was not
associated with the modulation of Bcl-2, Bax, or Mcl-1 levels,
but was associated with the cleavage of the antiapoptotic
protein Bcl-XL to a proapoptotic 18-kD form. This cleavage
of Bcl-XL was dependent on caspase-3 activation since Bcl-XL cleavage and apoptosis were inhibited by the
caspase-3 inhibitor Z-DVED-fmk. CD437 markedly inhibited the
growth of WSU-CLL cells in severe combined immunodeficiency
(SCID) mice. Tumor growth inhibition, growth delay, and log
cell kill were 85.7%, 21 days, and 2.1, respectively, in the
treated mice. Moreover, 1 of the 5 treated mice was tumor-free longer
than 150 days and thus was considered cured. Exposure of primary
cultures of both B-CLL and ALL cells obtained from patients to CD437
and MM002 resulted in their apoptosis. These results suggest that CD437
and MM002 analogs may have a potential role in the treatment
of B-CLL and ALL.
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