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首页> 外文期刊>Biomedicine & pharmacotherapy =: Biomedecine & pharmacotherapie >The reduction of IL-6 gene expression, pAKT, pERK1/2, pSTAT3 signaling pathways and invasion activity by gallic acid in prostate cancer PC3 cells
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The reduction of IL-6 gene expression, pAKT, pERK1/2, pSTAT3 signaling pathways and invasion activity by gallic acid in prostate cancer PC3 cells

机译:没食子酸可降低前列腺癌PC3细胞IL-6基因表达,pAKT,pERK1 / 2,pSTAT3信号通路和侵袭活性

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Prostate cancer (PC) is one of the most common cancers among men. Progression of prostate cancer is associated with an increase in cellular level of interleukin-6 (IL-6). Gallic acid (GA) is a polyhydroxy phenolic compound which can inhibit the growth of cancer cells. The aim of this study was to evaluate the effects of GA treatment on cell viability, proliferation, invasion, IL-6 gene expression, IL-6 secretion, cellular levels of pSTAT3, pERK1/2, and pAKT signaling proteins in human prostate cancer PC3 cells. PC3 cells viability after treatment with GA (0-120 mM) was evaluated by 3-(4,5-dimethylthiazol-2-yl)-2,5diphenyltetrazolium bromide (MTT) assay. The expression of IL-6 was investigated using real-time polymerase chain reaction. Cellular concentration of pSTAT3, pERK1/2, and pAKT signaling proteins were determined by Western blotting technic. PC3 cells invasion was assessed by invasion assay test. Treatment with GA caused a significant decrease in cell viability, proliferation, invasion, cellular levels of pSTAT3, pERK1/2, and pAKT signaling proteins after 48 h in a dose-dependent manner. The level of IL-6 and its gene expression decreased significantly in PC3 cells treated with GA. Our results show that IL-6 down-regulation and decreased IL-6 protein level in PC3 cells by GA resulted in diminishing of pSTAT3, pERK1/2, and pAKT signaling proteins which lead to the reduction of the cell survival, proliferation, and invasion in PC3 cells. Therefore, it seems that GA can be considered an anticancer agent in the treatment of prostate cancer. (C) 2016 Elsevier Masson SAS. All rights reserved.
机译:前列腺癌(PC)是男性中最常见的癌症之一。前列腺癌的进展与白细胞介素6(IL-6)的细胞水平升高有关。没食子酸(GA)是一种多羟基酚类化合物,可以抑制癌细胞的生长。这项研究的目的是评估GA治疗对人前列腺癌PC3细胞活力,增殖,侵袭,IL-6基因表达,IL-6分泌,pSTAT3,pERK1 / 2和pAKT信号蛋白细胞水平的影响。细胞。通过3-(4,5-二甲基噻唑-2-基)-2,5-二苯基四唑溴化物(MTT)测定法评估用GA(0-120 mM)处理后PC3细胞的生存能力。使用实时聚合酶链反应研究了IL-6的表达。通过Western印迹技术确定pSTAT3,pERK1 / 2和pAKT信号蛋白的细胞浓度。通过侵袭试验测试评估PC3细胞的侵袭。在48小时后,用GA进行治疗后,细胞活力,增殖,侵袭,pSTAT3,pERK1 / 2和pAKT信号蛋白的细胞水平显着降低,且呈剂量依赖性。 GA处理的PC3细胞中IL-6的水平及其基因表达显着降低。我们的结果表明,GA可使PC3细胞中IL-6下调并降低IL-6蛋白水平,从而导致pSTAT3,pERK1 / 2和pAKT信号蛋白减少,从而导致细胞存活,增殖和侵袭减少。在PC3细胞中。因此,似乎GA可以被认为是治疗前列腺癌的抗癌剂。 (C)2016 Elsevier Masson SAS。版权所有。

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