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Blood, 15 November 2000, Vol. 96, No. 10, pp. 3553-3559
NEOPLASIA
HIV-1 protease inhibitors decrease proliferation and induce
differentiation of human myelocytic leukemia cells
Takayuki Ikezoe,
Eric S. Daar,
Jun-ichi Hisatake,
Hirokuni Taguchi, and
H.
Phillip Koeffler
From the Division of Hematology/Oncology, Infectious
Disease, Cedars-Sinai Research Institute, UCLA School of Medicine, Los
Angeles, CA; Department of Internal Medicine, Kochi Medical School,
Kochi, Japan.
Inhibitors of the protease of human immunodeficiency virus
type 1 (HIV-1) may inhibit cytoplasmic retinoic acid-binding proteins, cytochrome P450 isoforms, as well as P-glycoproteins. These features of
the protease inhibitors might enhance the activity of retinoids. To
explore this hypothesis, myeloid leukemia cells were cultured with
all-trans retinoic acid (ATRA) either alone or in
combination with the HIV-1 protease inhibitors indinavir, ritonavir,
and saquinavir. Consistent with the hypothesis, the HIV-1 protease
inhibitors enhanced the ability of ATRA to inhibit growth and induce
differentiation of HL-60 and NB4 myeloid leukemia cells, as measured by
expression of CD11b and CD66b cell surface antigens, as well as
reduction of nitroblue tetrazolium. Growth of ATRA-resistant UF-1 cells was also inhibited when cultured with the combination of ATRA and
indinavir. Moreover, indinavir enhanced the ability of ATRA to induce
expression of the myeloid differentiation-related transcription factor
C/EBP messenger RNA in NB4 cells by 9.5-fold. Taken together, the
results show that HIV-1 protease inhibitors enhance the
antiproliferative and differentiating effects of ATRA on myeloid
leukemia cells. An HIV-1 protease inhibitor might be a useful adjuvant
with ATRA for patients with acute promyelocytic leukemia and possibly
retinoid-resistant cancers.
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