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首页> 外文期刊>Life sciences >Emodin-induced apoptosis through p53-dependent pathway in human hepatoma cells
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Emodin-induced apoptosis through p53-dependent pathway in human hepatoma cells

机译：大黄素通过p53依赖性途径诱导人肝癌细胞凋亡

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Most of the commonly used cytotoxic anticancer drugs have been shown to induce apoptosis in susceptible cells. However, the signaling pathway of their apoptotic effects remains undefined. In this study, the cytotoxic effect of emodin on various human hepatoma cell lines was investigated. Results demonstrated that emodin exhibited strongly suppressing effect on HepG2/C3A, PLC/PRF/5, and SK-HEP-1 cells, with the IC50 value of 42.5, 46.6, and 53.1 muM, respectively. Furthermore, emodin induced apoptosis in HepG2/C3A cells was clearly verified by the appearance of DNA fragmentation and sub-G, accumulation. Besides, HepG2/C3A cells were found to be arrested in G(2)/M phase after the cells were treated with 60 muM emodin for 48 h. Moreover, significant increase in the levels of apoptosis-related signals such as p53 (419.3 mug/ml), p21 (437.4 units/ml), Fas (6.6 units/ml), and caspase-3 (35.4 pmol/min) were observed in emodin treated HepG2/C3A cells. Taken together, emodin displays effective inhibitory effects on the growth of various human hepatoma cell lines and stimulates the expression of p53 and p21 that resulted in the cell cycle arrest of HepG2/C3A cells at G2/M phase. Results also suggest that emodin-induced apoptosis in HepG2/C3A cells were mediated through the activation of p53, p21, Fas/APO-1, and caspase-3. It implies that emodin could be a useful chemotherapeutical agent for treatment of hepatocellular carcinoma (HCC). (C) 2004 Elsevier Inc. All rights reserved. [References: 36]
机译：已显示大多数常用的细胞毒性抗癌药可诱导易感细胞凋亡。然而，其凋亡作用的信号传导途径仍然不确定。在这项研究中，研究了大黄素对各种人类肝癌细胞系的细胞毒性作用。结果表明，大黄素对HepG2 / C3A，PLC / PRF / 5和SK-HEP-1细胞具有强烈的抑制作用，IC50值分别为42.5、46.6和53.1μM。此外，大黄素诱导的HepG2 / C3A细胞凋亡通过DNA片段的出现和亚G的积累得以明确证实。此外，在用60μM大黄素处理48 h后，发现HepG2 / C3A细胞被阻滞在G（2）/ M期。此外，观察到凋亡相关信号的水平显着增加，例如p53（419.3 mug / ml），p21（437.4单位/ ml），Fas（6.6单位/ ml）和caspase-3（35.4 pmol / min）。在大黄素处理过的HepG2 / C3A细胞中。总之，大黄素对各种人类肝癌细胞系的生长均表现出有效的抑制作用，并刺激p53和p21的表达，从而导致HepG2 / C3A细胞在G2 / M期的细胞周期停滞。结果还表明，大黄素诱导的HepG2 / C3A细胞凋亡是通过激活p53，p21，Fas / APO-1和caspase-3介导的。这表明大黄素可能是治疗肝细胞癌（HCC）的有用化学治疗剂。 （C）2004 Elsevier Inc.保留所有权利。 [参考：36]

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