Genistein Promotes Proliferation of Human Cervical Cancer Cells Through Estrogen Receptor-Mediated PI3K/Akt-NF-κB Pathway.
Genistein Promotes Proliferation of Human Cervical Cancer Cells Through Estrogen Receptor-Mediated PI3K/Akt-NF-κB Pathway.
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金雀异黄素通过雌激素受体介导的 PI3K/Akt-NF-κB 途径促进人宫颈癌细胞增殖
DOI：
10.7150/jca.20499
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发表时间：
2018
影响因子：
3.9
通讯作者：
Xie MY
中科院分区：
文献类型：
--
作者：
Chen HH;Chen SP;Zheng QL;Nie SP;Li WJ;Hu XJ;Xie MY
植物雌激素是一类与17β-雌二醇（E2）结构相似的多酚类化合物，是女性体内主要的雌激素。因此，植物雌激素可能会影响生殖和内分泌系统，导致雌激素相关癌症的发展。染料木黄酮（Gen）是研究最多的植物雌激素之一，对人宫颈癌细胞（HeLa）的影响，在这项研究中。结果表明，Gen在0.001、0.01、0.1和1 μmol·L-1浓度下均能促进HeLa细胞的增殖，并呈剂量依赖性。Gen使S期细胞比例增加，G1期细胞比例减少。此外，Gen处理组细胞凋亡率明显低于对照组。同时发现，Gen可激活ERα、Akt和核NF-κB p65蛋白的表达，三者之间的相关性可能是：ERα在前，Akt在后，核NF-κB p65蛋白在后。此外，核NF-κB B p65下游基因的激活与肿瘤细胞的细胞周期和凋亡有关。本研究结果提示Gen可能通过雌激素受体介导的PI 3 K/Akt-NF-κB通路及进一步激活核NF-κB p65下游基因促进细胞增殖。
Phytoestrogens are polyphenol compounds which have similar structure to 17β-estradiol (E2), a kind of main estrogen in women. Thus, phytoestrogens may affect the reproductive and endocrine systems, leading to the development of estrogen-related cancers. The effect of genistein (Gen), one of the most studied phytoestrogens, on human cervical cancer cells (HeLa) was investigated in this study. It was found that Gen at concentrations of 0.001, 0.01, 0.1 and 1 µmol·L-1 promoted the proliferation of HeLa cells in a dose-dependent manner. Gen increased the portion of HeLa cells in S phase and decreased the portion of the cells in G1 phase. Besides, apoptosis rate of the cells was significantly lower when treated with Gen compared with the control group. It was also found that the expression of ERα, Akt or nuclear NF-κB p65 protein was activated by Gen. The correlation between these three proteins may be as following: ERα was the upstream, followed by Akt, and then nuclear NF-κB p65 protein. In addition, the downstream genes of activated nuclear NF-κB p65 were found to be associated with cell cycle and apoptosis of cancer cells. Our results suggested that Gen may stimulate cell proliferation partially through the estrogen receptor-mediated PI3K/Akt-NF-κB pathway and the further activation of the downstream genes of nuclear NF-κB p65.
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