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(-)-表没食子儿茶素-3-没食子酸酯通过非依赖于 67 kDa 层粘连蛋白受体诱导白血病细胞发生非凋亡性死亡。

(-)-Epigallocatechin-3-O-gallate induces nonapoptotic cell death in leukemia cells independent of the 67 kDa laminin receptor.

机构信息

Department of Radiological Life Sciences, Hirosaki University Graduate School of Health Sciences, 66-1 Hon-cho, Hirosaki, Aomori 036-8564, Japan.

出版信息

J Nat Prod. 2011 Apr 25;74(4):695-700. doi: 10.1021/np1007729. Epub 2011 Mar 24.

Abstract

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 cell growth of HL60 myeloid leukemia cells and Raji 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 1 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.

摘要

67 kDa 层粘连蛋白受体 (67LR) 介导 (-)-表没食子儿茶素-3-O-没食子酸酯 (1; EGCG) 仅在生理浓度下发挥 67LR 直接作用。采用流式细胞术分析,研究了生理浓度 1 对髓系和淋巴白血病细胞的生物学效应与 67LR 的相关性。结果表明,生理浓度 1 可抑制 HL60 髓系白血病细胞和 Raji 淋巴白血病细胞的生长,而与 67LR 表达无关。此外,细胞内活性氧水平、凋亡特征如磷脂酰丝氨酸易位和活化的 caspase-3 没有明显变化。生理浓度 1 的活性不依赖于直接的 67LR 介导作用,并且该化合物诱导早幼粒细胞白血病和非霍奇金淋巴瘤细胞发生类似坏死的死亡。

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