Arsenic induces apoptosis in B-cell leukaemic cell lines in vitro: activation of caspases and down-regulation of Bcl-2 protein
Arsenic induces apoptosis in B-cell leukaemic cell lines in vitro: activation of caspases and down-regulation of Bcl-2 protein
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DOI：
10.1046/j.1365-2141.1998.00869.x
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发表时间：
1998-09-01
影响因子：
6.5
通讯作者：
Yagi, K
中科院分区：
文献类型：
--
作者：
Akao, Y;Mizoguchi, H;Yagi, K
我们发现砷在体外对11个不同细胞系的4个B细胞白血病细胞系的细胞生长有抑制作用。其中两株系KOCL44和LyH7通过形态和核小体DNA片段化研究发现细胞发生了凋亡。在四个生长受抑的B细胞系中，有三个是带有t(11：19)(q23；p13)易位的急性婴儿白血病，涉及编码转录因子三胸果蝇的MLL基因。Western印迹和酶学分析发现，砷诱导的KOCL44和LyH7细胞的凋亡与caspase有关。Western印迹分析显示，在LyH7细胞凋亡过程中，Bcl2的表达减少。我们的结论是，caspase的激活和bcl2的下调共同决定了B细胞白血病细胞对砷的反应的命运。
We showed that arsenic inhibited the cell growth of four B-cell leukaemia cell lines of 11 various cell lines in vitro. In two of these four lines, KOCL44 and LyH7, apoptosis was identified by morphological and nucleosomal DNA fragmentation studies. Three of the four B-cell lines that were growth inhibited were acute infantile leukaemia with t(11:19)(q23;p13) translocations involving the MLL gene that encodes the transcriptional factor Drosophila trithorax. The arsenic-induced apoptosis in KOCL44 and LyH7 cells was found to be linked to caspases by Western blot and enzymological analyses. The amount of Bcl-2 was reduced during apoptosis in LyH7 as judged by Western blot analysis. We concluded that combined activation of the caspases and down-regulation of Bcl-2 could determine the fate of B-cell leukaemic cells in response to arsenic.