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首页> 外文期刊>Life sciences >Isoliquiritigenin induces apoptosis and cell cycle arrest through p53-dependent pathway in Hep G2 cells
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Isoliquiritigenin induces apoptosis and cell cycle arrest through p53-dependent pathway in Hep G2 cells

机译：异寡糖原蛋白通过p53依赖性途径诱导Hep G2细胞凋亡和细胞周期停滞

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摘要

Isoliquiritigenin (ISL) is a natural pigment with the simple chalcone structure 4,2',4'-trihydroxychalcone. In this study, we report ISL induced inhibition in the proliferation of human hepatoma cells (Hep G2) for the first time. The cell proliferation inhibition achieved by ISL treatment resulted in a G2/M-phase arrest and programmed cell death. ISL treatment was found to result in the upregulation of p53, p21/WAF1, Fas/APO-1 receptor, Fas ligand, Bax and NOXA, but not in Bad. To elevate the role of p53 in these functions, we generated Hep G2 cells that express the dominant negative p53, which blocks the transcriptional activity of p53. The enhancement of p21/WAFI, Fas/APO-1, Bax and NOXA were decreased in Hep 02 cells that lack functional p53. Furthermore, Hep G2 cells were significantly more resistant to ISL when the activity of p53 was blocked. These results demonstrated that ISL-inducible p53 plays a key apoptotic role, and may do so by regulating the expression of specific target molecules that promotes efficient apoptotic cell death following G2/M-cell cycle arrest. (c) 2005 Elsevier Inc. All rights reserved.
机译：异quiritigeninin（ISL）是具有简单查尔酮结构的4,2'，4'-三羟基查尔酮的天然色素。在这项研究中，我们首次报道了ISL诱导的人肝癌细胞（Hep G2）增殖抑制作用。通过ISL处理实现的细胞增殖抑制导致G2 / M期停滞和程序性细胞死亡。发现ISL处理可导致p53，p21 / WAF1，Fas / APO-1受体，Fas配体，Bax和NOXA上调，但Bad则不起作用。为了提升p53在这些功能中的作用，我们生成了表达显性负性p53的Hep G2细胞，该细胞阻断了p53的转录活性。在缺乏功能性p53的Hep 02细胞中，p21 / WAFI，Fas / APO-1，Bax和NOXA的增强降低。此外，当p53的活性被阻断时，Hep G2细胞对ISL的抵抗力明显增强。这些结果表明，ISL诱导型p53发挥关键的凋亡作用，并且可以通过调节特异性靶分子的表达来发挥作用，该分子在G2 / M细胞周期停滞后促进有效的凋亡细胞死亡。 （c）2005 Elsevier Inc.保留所有权利。

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