Induction of apoptosis in HL-60 cells by eicosapentaenoic acid (EPA) is associated with downregulation of bcl-2 expression.
Dietary polyunsaturated fatty acids (PUFAs) have been reported as a potential group of natural products which modulate tumor cell growth. In present study, eicosapentaenoic acid (EPA) was found to inhibit proliferation of human leukemic HL-60 and K-562 cells in vitro. EPA arrested cell cycle progression at G0/G1 phase, and induced necrosis in both HL-60 and K-562 cells. However, EPA induced apoptosis only in HL-60 but not K-562 cells. Also, bcl-2 protein expression was downregulated in much greater extent than that of bax showing that depression of bcl-2 might be an important step during the EPA-induced apoptosis in HL-60 cells.
Chiu
L C
LC
Department of Zoology, The University of Hong Kong, People's Republic of China. b100952@mailserv.cuhk.edu.hk
Wan
J M
JM
D017209:Apoptosis / Q000187:drug effects*; D015536:Down-Regulation; D004354:Drug Screening Assays, Antitumor; D015118:Eicosapentaenoic Acid / Q000494:pharmacology*; D005434:Flow Cytometry; D016193:G1 Phase / Q000187:drug effects; D018922:HL-60 Cells; D006801:Humans; D015464:Leukemia, Myelogenous, Chronic, BCR-ABL Positive / Q000188:drug therapy* / Q000473:pathology; D015473:Leukemia, Promyelocytic, Acute / Q000188:drug therapy* / Q000473:pathology; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000096:biosynthesis*; D016192:Resting Phase, Cell Cycle / Q000187:drug effects; D014407:Tumor Cells, Cultured
D019253:Proto-Oncogene Proteins c-bcl-2; D015118:Eicosapentaenoic Acid