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首页> 外文期刊>Oncology letters >Role of Ku70 and Bax in epigallocatechin-3-gallate-induced apoptosis of A549 cells in vivo
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Role of Ku70 and Bax in epigallocatechin-3-gallate-induced apoptosis of A549 cells in vivo

机译：Ku70和Bax在表没食子儿茶素-3-没食子酸酯诱导的A549细胞凋亡中的作用

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摘要

EGCG (epigallocatechin-3-gallate), the major catechin found in green tea, has been demonstrated to inhibit proliferation and induce apoptosis in a number of types of tumors. Recent studies reveal that EGCG has various anticancer effects. This study investigated a further possible molecular mechanism of the anticancer effects of EGCG in murine lung cancer xenografts. In the study, A549 human lung cancer cells were injected into nude mice. Tumor volume was used to measure cancer cell growth. The weight of the animals was used to assess the toxicity of the drugs. The expression of protein and mRNA was assayed by western blot analysis and RT-PCR, respectively. The interaction between Bax and Ku70 was determined by immunoprecipitation. Our results suggest that EGCG induced A549 lung cancer cell apoptosis in vivo, and had less toxic effects compared to classical anticancer drugs. EGCG may inhibit the surrogate markers of proliferation and apoptosis (caspase 3) in A549 tumor xenografts in vivo. In addition, EGCG downregulated the expression of Bcl-xl and upregulated the expression of Bax mRNA and protein. Further experiments indicated that EGCG downregulated the protein expression of Ku70 and interrupted the binding of Ku70 and Bax. This is the first study demonstrating that the induction of apoptosis by EGCG may be caused by the downregulation of Ku70 and that EGCG disrupts the interaction between Ku70 and Bax in lung cancer.
机译：绿茶中发现的主要儿茶素EGCG（epigallocatechin-3-gallate）已被证明可抑制多种类型肿瘤的增殖并诱导细胞凋亡。最近的研究表明，EGCG具有多种抗癌作用。这项研究调查了EGCG在鼠肺癌异种移植物中抗癌作用的进一步可能的分子机制。在这项研究中，将A549人肺癌细胞注射入裸鼠。肿瘤体积用于测量癌细胞的生长。使用动物的体重来评估药物的毒性。蛋白和mRNA的表达分别通过蛋白质印迹分析和RT-PCR进行测定。 Bax和Ku70之间的相互作用是通过免疫沉淀法确定的。我们的结果表明，EGCG在体内可诱导A549肺癌细胞凋亡，并且与传统抗癌药物相比，毒性作用较小。 EGCG可能在体内抑制A549肿瘤异种移植物中增殖和凋亡的替代标志物（胱天蛋白酶3）。此外，EGCG下调Bcl-xl的表达，并上调Bax mRNA和蛋白的表达。进一步的实验表明，EGCG下调了Ku70的蛋白表达，并中断了Ku70与Bax的结合。这是第一项证明EGCG诱导细胞凋亡的研究，可能是由于Ku70的下调引起的，并且EGCG破坏了肺癌中Ku70与Bax之间的相互作用。

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