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Effect of n-3 and n-6 fatty acids on proliferation and differentiation of
promyelocytic leukemic HL-60 cells
HS Finstad, SO Kolset, JA Holme, R Wiger, AK Farrants, R Blomhoff and CA Drevon
Section for Dietary Research, Institute of Nutrition Research, University
of Oslo, Norway.
Promyelocytic leukemic HL-60 cells were incubated with different fatty
acids. Arachidonic acid (AA; 20:4, n-6) and eicosapentaenoic acid (EPA;
20:5, n-3) were the most potent inhibitors of proliferation in a dose-
dependent way. Retinoic acid (RA) was used as a positive control.
Inhibitors of cyclooxygenase and lipoxygenase or addition of antioxidants
did not influence the effect of EPA or AA on cell proliferation. Increased
capacity to generate superoxide anions after phorbol ester treatment and a
reduced serglycin messenger RNA level in cells treated with AA or EPA
indicated that these fatty acids induced differentiation in HL-60 cells
similar to that induced by RA. However, down-regulation of the c-myc mRNA
level, also typical for differentiation with RA in HL-60 cells, was not
observed in cells incubated with AA or EPA. Flow cytometric analyses showed
that in cultures incubated with AA or EPA, the proportion of cells in the
G1 phase of the cell cycle increased. Similar effects were observed with
RA. By flow cytometry and light scatter analyses it could be shown that AA
made 8% of the cells apoptotic and 7% necrotic. The corresponding numbers
were 21% and 10% for RA-treated cells, and 19% and 32% for EPA- treated
cells. The present study shows that AA and EPA reduce the proliferation
rate of HL-60 cells. This is mediated by mechanisms independent of
eicosanoids or lipid peroxidation products and is due to effects both on
apoptosis/necrosis and cell differentiation.
Volume 84,
Issue 11,
pp. 3799-3809,
12/01/1994
Copyright © 1994 by The American Society of Hematology
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