(-)-Epigallocatechin-3-O-gallate Induces Nonapoptotic Cell Death in Leukemia Cells Independent of the 67 kDa Laminin Receptor
(-)-Epigallocatechin-3-O-gallate Induces Nonapoptotic Cell Death in Leukemia Cells Independent of the 67 kDa Laminin Receptor
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DOI：
10.1021/np1007729
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发表时间：
2011-04-01
影响因子：
5.1
通讯作者：
Kashiwakura, Ikuo
中科院分区：
文献类型：
--
作者：
Hazawa, Masaharu;Takahashi, Kenji;Kashiwakura, Ikuo
67 kDa的层粘连蛋白受体(67 LR)仅在生理浓度时介导(-)-表没食子儿茶素没食子酸酯(1；EGCG)-67 LR的直接作用。用流式细胞术分析了生理浓度1对髓系白血病细胞和淋巴细胞白血病细胞的生物学效应与67-LR的相关性。结果表明，生理浓度的1抑制HL60髓性白血病细胞和Rap淋巴细胞性白血病细胞的生长，而不依赖于67LR的表达。细胞内活性氧水平、磷脂酰丝氨酸转位、caspase-3活化等细胞凋亡特征未见明显变化。在生理浓度下，I的活性不依赖于67LR介导的直接作用，这种化合物可以诱导早幼粒细胞白血病和非霍奇金淋巴瘤细胞的坏死性死亡。
The 67 kDa laminin receptor (67 LR) mediates (-)-epigallocatechin-3-O-gallate (1; EGCG)-67 LR direct action only at physiological concentrations. The relevancy of biological effects of 1 at physiological concentrations to 67 LR was investigated in myeloid and lymphoid leukemia cells using flow cytometric analysis. It was shown that physiological concentrations of 1 suppressed the tell growth of HL60 myeloid leukemia cells and Rap lymphoid leukemic cells independent of 67 LR expression. Moreover, there was no discernible change in the levels of intracellular reactive oxygen species, characteristics Of apoptosis such as phosphatidylserine translocation and activated caspase-3. The activity of I at physiological concentrations does not depend, on direct 67 LR-mediated, actions, and this compound induces necrosis-like death of promyelocytic leukemia and non Hodgkin's lymphoma cells.