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Fas receptor (CD95)-mediated apoptosis is induced in leukemic cells
entering G1B compartment of the cell cycle
Y Komada, YW Zhou, XL Zhang, HL Xue, H Sakai, S Tanaka, H Sakatoku and M Sakurai
Department of Pediatrics, Mie University School of Medicine, Japan.
Apoptotic cell death induced by cross-linking Fas receptor (FasR/CD95) has
been investigated in human acute myelogenous leukemia (AML) cells.
FasR-mediated growth inhibition and DNA fragmentation could be induced in
certain cases of AML. Interestingly, when DNA synthesis and G1 -> S
transition in the cell cycle were enhanced by interleukin-3 or
granulocyte-macrophage colony-stimulating factor, Fas-insensitive blast
cells acquired cellular susceptibility toward FasR-mediated growth
inhibition. To further evaluate an association between the Fas-R- mediated
action and a specific phase of the cell cycle, a FasR+ leukemic cell line,
MML-1, was established from a patient with AML. The morphologic feature of
dying cells and DNA fragmentation indicated that FasR cross-linking induced
apoptotic cell death in MML-1 cells. Cell cycle arrest in G1A phase with
the treatment of phorbol 12-myristate 13- acetate or thymidine rendered
MML-1 cells resistant to FasR-mediated apoptosis without downregulation of
surface FasR expression. However, S- phase arrest with 5-fluorouracil could
neither enhance nor inhibit FasR- mediated apoptosis. Simultaneous DNA/RNA
quantification analysis revealed the selective loss of cells in G1B
compartment, accompanied by the increase of apoptotic nuclei in sub-G1
fraction. These findings suggested that FasR-mediated apoptotic signals
could be transduced into cells in G1B compartment and G1A -> G1B
transition might augment the induction of FasR-mediated apoptosis.
Volume 86,
Issue 10,
pp. 3848-3860,
11/15/1995
Copyright © 1995 by The American Society of Hematology
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