In this study, we have evaluated the chemopreventive role of
aloe-emodin in human promyelocytic
leukemia HL-60 cells in vitro by studying the regulation of proliferation, cell cycle and apoptosis.
Aloe-emodin inhibited cell proliferation and induced G2/M arrest and apoptosis in HL-60 cells. Investigation of the levels of
cyclins B1, E and A by immunoblot analysis showed that
cyclin E level was unaffected, whereas
cyclin B1 and A levels increased with
aloe-emodin in HL-60 cells. Investigation of the levels of
cyclin-dependent kinases, Cdk1 and 2, showed increased levels of Cdk1 but the levels of Cdk2 were not effected with
aloe-emodin in HL-60 cells. The levels of p27 were increased after HL-60 cells were cotreated with various concentrations of
aloe-emodin. The increase of the levels of p27 may be the major factor for
aloe-emodin to cause G2/M arrest in these examined cells. Flow cytometric assays and DNA fragmentation gel electrophoresis also confirmed
aloe-emodin induced apoptosis in HL-60 cells. The levels of
caspase-3 were increased after HL-60 cells were cotreated with 10 microM
aloe-emodin for 12, 24, 48, and 72 hours. Taken together,
aloe-emodin therefore appears to exert its anticarcinogenesis properties by inhibiting proliferation and inducing cell cycle arrest and apoptosis underwent activation of
caspase-3 in human
leukemia HL-60 cells.