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Dysregulated bcl-2 expression inhibits apoptosis but not differentiation of
retinoic acid-induced HL-60 granulocytes
JR Park, K Robertson, DD Hickstein, S Tsai, DM Hockenbery and SJ Collins
Program in Molecular Medicine, Fred Hutchinson Cancer Research Center,
Seattle, WA 98104.
The bcl-2-proto-oncogene appears to contribute to the development of
certain malignancies by inhibiting programmed cell death (apoptosis).
Mature granulocytes show a markedly limited life span and rapidly undergo
apoptosis. To further define the relationship between apoptosis and
granulocyte differentiation, we used retroviral vector-mediated gene
transduction to introduce the normal bcl-2 gene into the HL-60 myeloid
leukemia cell line and determined the response of these bcl-2- transduced
HL-60 cells to the induction of granulocyte differentiation by retinoic
acid (RA). Although the bcl-2-transduced HL-60 cells showed the same
differentiative response to RA as did the parental HL-60 cells, the life
span of the RA-induced, bcl-2-transduced HL-60 granulocytes was markedly
prolonged compared with that of the RA- induced parental HL-60
granulocytes. DNA fragmentation studies indicate that this prolonged life
span resulted from diminished apoptosis in the bcl-2-transduced cells.
These studies indicate that bcl-2 is involved in regulating apoptosis in
maturing granulocytes. Because bcl-2 over- expression did not interfere
with RA-induced granulocyte differentiation, it appears that granulocyte
differentiation and apoptosis are under distinct and separate regulatory
controls.
Volume 84,
Issue 2,
pp. 440-445,
07/15/1994
Copyright © 1994 by The American Society of Hematology
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