环氧二十碳三烯酸（EPA）通过 Pyk2 通路和活性氧（ROS）对前列腺癌细胞 PC3 的抗癌作用。
Contribution of Pyk2 pathway and reactive oxygen species (ROS) to the anti-cancer effects of eicosapentaenoic acid (EPA) in PC3 prostate cancer cells.
机构信息
Laboratory of Physiology, Faculty of Pharmaceutical Sciences, Josai University, 1-1 Keyakidai, Sakado, Saitama, 350-0295, Japan.
Laboratory of Clinical Pathology, Faculty of Pharmaceutical Sciences, Josai University, 1-1 Keyakidai, Sakado, Saitama, 350-0295, Japan.
出版信息
Lipids Health Dis. 2020 Jan 31;19(1):15. doi: 10.1186/s12944-019-1122-4.
BACKGROUND
n-3 polyunsaturated fatty acids (n-3 PUFAs), including eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), are thought to exert protective effects in cardiovascular diseases. In addition, n-3 PUFAs have demonstrated anti-cancer effects in vitro and in vivo.
OBJECTIVE
We investigated the anti-cancer effects and mechanism of action of EPA on PC3 prostate cancer cells in vitro.
METHODS
PC3 cells were treated with various concentrations of EPA, and cell survival and the abilities of migration and invasion were evaluated. The time course of the growth inhibitory effect of EPA on PC3 cells was also assessed. The mechanism underlying the anti-cancer effects of EPA was investigated by human phosphokinase and human apoptosis antibody arrays, and confirmed by western blot analysis. We also examined the contribution of reactive oxygen species (ROS) to the effects of EPA using the ROS inhibitor N-acetyl cysteine.
RESULTS
EPA decreased the survival of PC3 cells in a dose-dependent manner within 3 h of application, with an effective concentration of 500 μmol/L. EPA inhibited proline-rich tyrosine kinase (Pyk)2 and extracellular signal-regulated kinase 1/2 phosphorylation as determined by western blotting and the antibody arrays. The growth of PC3 cells was inhibited by EPA, which was dependent on ROS induction, while EPA inhibited Pyk2 phosphorylation independent of ROS production.
CONCLUSIONS
Inhibition of Pyk2 phosphorylation and ROS production contribute to the anticancer effects of EPA on PC3 cells.
背景
n-3 多不饱和脂肪酸（n-3 PUFAs），包括二十碳五烯酸（EPA）和二十二碳六烯酸（DHA），被认为对心血管疾病具有保护作用。此外，n-3 PUFAs 在体外和体内均显示出抗癌作用。
目的
我们研究了 EPA 对 PC3 前列腺癌细胞的体外抗癌作用和作用机制。
方法
用不同浓度的 EPA 处理 PC3 细胞，评估细胞存活以及迁移和侵袭能力。还评估了 EPA 对 PC3 细胞生长抑制作用的时间过程。通过人磷酸激酶和人凋亡抗体阵列研究了 EPA 的抗癌作用机制，并通过 Western blot 分析进行了确认。我们还使用活性氧（ROS）抑制剂 N-乙酰半胱氨酸研究了 ROS 对 EPA 作用的贡献。
结果
EPA 在应用后 3 小时内以剂量依赖性方式降低 PC3 细胞的存活率，有效浓度为 500μmol/L。Western blot 和抗体阵列分析表明，EPA 抑制脯氨酸丰富的酪氨酸激酶（Pyk）2 和细胞外信号调节激酶 1/2 的磷酸化。EPA 抑制 PC3 细胞的生长，这依赖于 ROS 的诱导，而 EPA 抑制 Pyk2 磷酸化而不依赖于 ROS 的产生。
结论
抑制 Pyk2 磷酸化和 ROS 产生有助于 EPA 对 PC3 细胞的抗癌作用。
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