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The upregulation of Myb and Peg3 may mediate EGCG inhibition effect on mouse lung adenocarcinoma

机译:Myb和Peg3的上调可能介导EGCG对小鼠肺腺癌的抑制作用

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The antioxidant activity of green tea polyphenol epigallocatechin-3-gallate (EGCG) has been found to be critical in inhibiting carcinogenesis. In our previous study, we identified a set of protein coding genes and microRNAs whose expressions were significantly modulated in response to the EGCG treatment in tobacco carcinogen-induced lung adenocarcinoma in A/J mice. In this study, we further conducted some statistical analysis on our microarray data and employed The Cancer Genome Atlas (TCGA) lung adenocarcinoma datasets as additional control. We postulated that if a gene mediates EGCG's cancer inhibition, its expression level change caused by EGCG should be opposite to what occurred in the carcinogenesis. With this assumption, we identified Myb and Peg3 as the primary genes involved in the cancer inhibitory activities of EGCG.
机译:已发现绿茶多酚EpigallocateChin-3-gallate(EGCG)的抗氧化活性在抑制致癌物中是至关重要的。在我们以前的研究中,我们鉴定了一组蛋白质编码基因和MicroRNA,其表现的表现响应于A / J小鼠中的烟草致癌肺腺癌的EGCG处理而显着调节。在这项研究中,我们进一步对我们的微阵列数据进行了一些统计分析,并使用癌症基因组地图集(​​TCGA)肺腺癌数据集作为额外的控制。我们假设如果基因介导EGCG的癌症抑制,EGCG引起的表达水平变化应与致癌发生的发生相反。凭借这种假设,我们将MyB和PEG3鉴定为患有EGCG癌症抑制活性的主要基因。

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