The antiproliferative activity of aloe-emodin is through p53-dependent and p21-dependent apoptotic pathway in human hepatoma cell lines
The antiproliferative activity of aloe-emodin is through p53-dependent and p21-dependent apoptotic pathway in human hepatoma cell lines
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DOI：
10.1016/s0024-3205(02)01900-8
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发表时间：
2002-09-06
期刊：
影响因子：
6.1
通讯作者：
Lin, CC
中科院分区：
文献类型：
--
作者：
Kuo, PL;Lin, TC;Lin, CC
本研究的目的是研究芦荟大黄素对两种人类肝癌细胞系 Hep G2 和 Hep 3B 的抗癌作用。我们观察到芦荟大黄素在两种检查的细胞系中均抑制细胞增殖并诱导细胞凋亡，但具有不同的抗增殖机制。在 Hep G2 细胞中，芦荟大黄素诱导 p53 表达，并伴有 p21 表达的诱导，这与细胞周期停滞在 G1 期相关。此外，芦荟大黄素还能显着增加Fas/APO1受体和Bax的表达。相比之下，在p53缺陷的Hep 3B细胞中，芦荟大黄素对细胞增殖的抑制作用是通过p21依赖性方式介导的，这种方式不会导致细胞周期停滞或增加Fas/APO1受体的水平，而是通过增强Bax的表达来促进芦荟大黄素诱导的细胞凋亡。这些发现表明芦荟大黄素可能有助于预防肝癌。 (C) 2002 Elsevier Science Inc. 保留所有权利。
The aim of this study is to investigate the anticancer effect of aloe-emodin in two human liver cancer cell lines, Hep G2 and Hep 3B. We observed that aloe-emodin inhibited cell proliferation and induced apoptosis in both examined cell lines, but with different the antiproliferative mechanisms. In Hep G2 cells, aloe-emodin induced p53 expression and was accompanied by induction of p21 expression that was associated with a cell cycle arrest in G1 phase. In addition, aloe-emodin had a marked increase in Fas/APO1 receptor and Bax expression. In contrast, with p53-deficient Hep 3B cells, the inhibition of cell proliferation of aloe-emodin was mediated through a p21-dependent manner that did not cause cell cycle arrest or increase the level of Fas/APO1 receptor, but rather promoted aloe-emodin induced apoptosis by enhancing expression of Bax. These findings suggest that aloe-emodin may be useful in liver cancer prevention. (C) 2002 Elsevier Science Inc. All rights reserved.