Ara-C INDUCED APOPTOSIS IN HUMAN MYELOID LEUKEMIA CELL LINE HL-60: INDUCING APOPTOSIS IS THE PRIMARY MECHANISM OF CHEMOTHERAPY
Abstract
Objective: To elucidate the pattern of chemotherapy drugs induced apoptosis and its role in chemotherapy of acute leukemia.
Methods: Apoptosis induced by Ara-C in human myeloid leukemia cell line HL-60 was investigated by applying light microscope, electron microscopy combined with DNA electrophoresis and flow cytometry analysis techniques.
Results: Apoptosis persisted throughout 36 h following addition of Ara-C with a gradual augmentation. Efficiency of apoptosis was enhanced in a dosedependent pattern, HL-60 treated with six other chemotherapy drugs and peripheral white blood cells from a AML case undergoing DA regimen chemotherapy exhibited typical DNA ladder pattern. Further investigation indicated that chemotherapy drugs apoptosis came into being possibly by downregulating the expression of c-myc and bcl-2 oncogenes.
Conclusion: Chemotherapy induced apoptosis is the primary mechanism of chemotherapy.
Methods: Apoptosis induced by Ara-C in human myeloid leukemia cell line HL-60 was investigated by applying light microscope, electron microscopy combined with DNA electrophoresis and flow cytometry analysis techniques.
Results: Apoptosis persisted throughout 36 h following addition of Ara-C with a gradual augmentation. Efficiency of apoptosis was enhanced in a dosedependent pattern, HL-60 treated with six other chemotherapy drugs and peripheral white blood cells from a AML case undergoing DA regimen chemotherapy exhibited typical DNA ladder pattern. Further investigation indicated that chemotherapy drugs apoptosis came into being possibly by downregulating the expression of c-myc and bcl-2 oncogenes.
Conclusion: Chemotherapy induced apoptosis is the primary mechanism of chemotherapy.