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All-trans retinoic acid reverses phorbol ester resistance in a human
myeloid leukemia cell line
KD Yang, T Mizobuchi, SM Kharbanda, R Datta, E Huberman, DW Kufe and RM Stone
Laboratory of Clinical Pharmacology, Dana-Farber Cancer Institute, Harvard
Medical School, Boston, MA 02115.
Treatment of human HL-60 leukemic cells with 12-O-tetradecanoylphorbol-
13-acetate (TPA) is associated with activation of protein kinase C (PKC)
and induction of monocytic differentiation. An HL-60 variant cell line,
termed HL-525, derived from long-term exposure to TPA (Homma et al, Proc
Natl Acad Sci USA 83: 7316, 1986) is resistant to TPA-induced
differentiation and displays decreased PKC beta expression compared with
the HL-60 parent line. However, this variant exhibits features of
granulocytic differentiation, including nitroblue tetrazolium reduction,
when exposed to all-trans retinoic acid (ATRA). Whereas treatment of HL-525
cells with ATRA or TPA alone had no effect on features of monocytic
differentiation, these agents in combination resulted in cellular adhesion,
nonspecific esterase staining, and induction of the c-fms (monocyte growth
factor receptor) gene. In order to measure PKC expression associated with
the reversal of TPA resistance by ATRA, we exposed HL-525 cells to ATRA and
analyzed PKC- mRNA and protein levels. Exposure of HL-525 cells to ATRA for
3 days resulted in induction of PKC beta transcripts, whereas there was
little change in PKC alpha mRNA levels. ATRA treatment was also associated
with an increase in PKC activity and an induction of cytosolic PKC beta
protein levels. These findings are consistent with the hypothesis that ATRA
reverses TPA resistance in HL-525 cells by enhancing the expression of PKC.
Volume 83,
Issue 2,
pp. 490-496,
01/15/1994
Copyright © 1994 by The American Society of Hematology
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