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二十碳五烯酸(EPA)诱导HL-60细胞凋亡与bcl-2表达下调有关。

Induction of apoptosis in HL-60 cells by eicosapentaenoic acid (EPA) is associated with downregulation of bcl-2 expression.

作者信息

Chiu L C, Wan J M

机构信息

Department of Zoology, The University of Hong Kong, People's Republic of China.

出版信息

Cancer Lett. 1999 Oct 18;145(1-2):17-27. doi: 10.1016/s0304-3835(99)00224-4.

DOI:10.1016/s0304-3835(99)00224-4
PMID:10530765
Abstract

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.

摘要

据报道,膳食多不饱和脂肪酸(PUFAs)是一类具有调节肿瘤细胞生长潜力的天然产物。在本研究中,发现二十碳五烯酸(EPA)在体外可抑制人白血病HL-60和K-562细胞的增殖。EPA使细胞周期进程停滞在G0/G1期,并诱导HL-60和K-562细胞发生坏死。然而,EPA仅诱导HL-60细胞凋亡,而不诱导K-562细胞凋亡。此外,bcl-2蛋白表达下调的程度远大于bax,这表明bcl-2的抑制可能是EPA诱导HL-60细胞凋亡过程中的重要一步。

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