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Retinoid induced apoptosis in leukemia cells through a retinoic acid
nuclear receptor-independent pathway
CA Hsu, AK Rishi, X Su-Li, TM Gerald, MI Dawson, C Schiffer, U Reichert, B Shroot, GC Poirer and JA Fontana
Department of Medicine and Cancer Center, University of Maryland at
Baltimore and the Baltimore VA Medical Center, USA.
Trans retinoic acid (RA) has proven to be a potent therapeutic agent in the
treatment of acute promyelocytic leukemia. Unfortunately, other subtypes of
acute myelogenous leukemia are resistant to the antiproliferative and
differentiating effects of RA. In this report, we describe a novel retinoid
6-[3-(1-adamantyl)-4-hydroxyphenyl]-2- naphthalene carboxylic acid (AHPN;
CD437) that not only totally inhibits the proliferation of RA-resistant
leukemic cell lines HL-60R and K562 but also induces apoptosis in these
cells. Exposure of HL-60R to CD437 results in the rapid (within 30 minutes)
increase of the cyclin-dependent kinase inhibitor p21(waf1/cip1) as well as
GADD45 mRNA. Manifestations of CD437-mediated programmed cell death are
noted within 2 hours, as indicated by both the cleavage and activation of
the CPP32 protease and cleavage of poly (ADP-ribose) polymerase. This is
followed by cleavage of bcl-2 and internucleosomal DNA degradation. HL- 60R
cells do not express the retinoid nuclear receptor RAR beta and RAR gamma
and express a truncated RAR alpha. Thus, CD437 induction of p21(waf1/cip1)
and GADD45 mRNAs and apoptosis occurs through a unique mechanism not
involving the retinoid nuclear receptors. CD437 represents a unique
retinoid with therapeutic potential in the treatment of myeloid leukemia.
Volume 89,
Issue 12,
pp. 4470-4479,
06/15/1997
Copyright © 1997 by The American Society of Hematology
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