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首页> 外文期刊>The Journal of Nutritional Biochemistry >Apigenin causes G(2)/M arrest associated with the modulation of p21(Cip1) and Cdc2 and activates p53-dependent apoptosis pathway in human breast cancer SK-BR-3 cells
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Apigenin causes G(2)/M arrest associated with the modulation of p21(Cip1) and Cdc2 and activates p53-dependent apoptosis pathway in human breast cancer SK-BR-3 cells

机译：芹菜素导致人乳腺癌SK-BR-3细胞中与p21（Cip1）和Cdc2的调节有关的G（2）/ M停滞并激活p53依赖性凋亡途径。

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We studied the effects of apigenin on the cell cycle distribution and apoptosis of human breast cancer cells and explored the mechanisms underlying these effects. We first investigated the antiproliferative effects in SK-BR-3 cells exposed to between 1 and 100 muM apigenin for 24, 48 and 72 h. Apigenin significantly inhibited cell proliferation at concentrations over 50 muM, regardless of exposure time (P<.05), and resulted in significant cell cycle arrest in the G(2)/M phase after 48 h of treatment at high concentrations (50 and 100 muM; P<.05). To investigate the regulatory proteins of cell cycle arrest affected by apigenin, we treated cells with 50 and 100 muM apigenin for 72 h. Apigenin caused a slight decrease in cyclin D and cyclin E expression, with no change in CDK2 and CDK4. In addition, the apigenin-induced accumulation of the cell population in the G(2)/M phase resulted in a decrease in CDK1 together with cyclin A and cyclin B. In an additional study, apigenin also increased the accumulation of p53 and further enhanced the level of p21(Cip1), with no change in p27(Kip1). The expression of Bax and cytochrome c of p53 downstream target was increased markedly at high concentration treatment over 50 muM apigenin. Based on our findings, the mechanism by which apigenin causes cell cycle arrest via the regulation of CDK1 and p21(Cip1) and induction of apoptosis seems to be involved in the p53-dependent pathway.
机译：我们研究了芹菜素对人乳腺癌细胞周期分布和凋亡的影响，并探讨了这些作用的潜在机制。我们首先研究了暴露于1至100μM芹菜素之间24、48和72 h的SK-BR-3细胞的抗增殖作用。在超过50μM的浓度下，无论暴露时间长短（P <.05），芹菜素都显着抑制细胞增殖，并在高浓度（50和100）处理48小时后导致G（2）/ M期细胞明显停滞。 muM; P <.05）。为了研究芹菜素对细胞周期停滞的调控蛋白，我们用50和100μM芹菜素处理细胞72小时。芹菜素引起细胞周期蛋白D和细胞周期蛋白E表达的轻微降低，而CDK2和CDK4没有变化。此外，芹菜素诱导的G（2）/ M期细胞群体积累导致CDK1以及细胞周期蛋白A和细胞周期蛋白B减少。在另一项研究中，芹菜素还增加了p53的积累并进一步增强p21（Cip1）的水平，而p27（Kip1）没有变化。在超过50μM芹菜素的高浓度处理下，p53下游靶标的Bax和细胞色素c的表达明显增加。根据我们的发现，芹菜素通过CDK1和p21（Cip1）的调节引起细胞周期停滞以及诱导细胞凋亡的机制似乎与p53依赖性途径有关。

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