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首页> 外文期刊>Molecular Carcinogenesis >Epigenetic modulation of the retinoid X receptor alpha by green tea in the azoxymethane-Apc Min/+ mouse model of intestinal cancer.
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Epigenetic modulation of the retinoid X receptor alpha by green tea in the azoxymethane-Apc Min/+ mouse model of intestinal cancer.

机译：绿茶在肠癌的Azoxymethane-Apc Min / +小鼠模型中对类维生素A X受体α的表观遗传调控。

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We investigated the possible mechanisms of inhibition of colorectal carcinogenesis by green tea (GT) in azoxymethane-treated (AOM) Apc(Min/+) mice. Mice received water or a 0.6% (w/v) solution of GT as the only source of beverage. GT treatment commenced at the 8th week of age and lasted for 8 wk. The treatment caused a statistically significant reduction in the number of newly formed tumors (28%, P < 0.05). Immunohistochemical analysis showed that GT decreased the levels of beta-catenin and its downstream target cyclin D1. To probe a mechanism, we further investigated the expression of retinoic X receptor alpha (RXR alpha) in AOM/Apc(Min/+) tumors. Our results show that RXR alpha is selectively downregulated in AOM/Apc(Min/+) mouse intestinal tumors. In contrast, other retinoic receptors including retinoic acid receptor alpha (RAR alpha), RAR beta, RXR beta, and RXR gamma were all expressed in Apc(Min/+) adenomas. Furthermore, our results show that RXR alpha downregulation is an early event in colorectal carcinogenesis and is independent of beta-catenin expression. GT significantly increased the protein levels of RXR alpha. In addition, RT-PCR analysis showed that GT induced a similar increase in the levels of RXR alpha mRNA. Genomic bisulfite treatment of colonic DNA followed by pyrosequencing of 24 CpG sites in the promoter region of RXR alpha gene showed a significant decrease in CpG methylation with GT treatment. The results suggest that a low concentration of GT is sufficient to desilence RXR alpha and inhibit intestinal tumorigenesis in the Apc(Min/+) mouse.
机译：我们调查了绿茶（GT）在乙氧甲烷处理（AOM）Apc（Min / +）小鼠中抑制结直肠癌发生的可能机制。小鼠接受水或GT的0.6％（w / v）溶液作为唯一的饮料来源。 GT治疗从年龄的第8周开始，持续8周。该治疗导致新形成的肿瘤数量有统计上的显着减少（28％，P <0.05）。免疫组织化学分析表明，GT降低了β-catenin及其下游靶细胞周期蛋白D1的水平。为了探索一种机制，我们进一步研究了AOM / Apc（Min / +）肿瘤中视黄酸X受体alpha（RXR alpha）的表达。我们的结果表明，RXRα在AOM / Apc（Min / +）小鼠肠道肿瘤中选择性下调。相反，其他视黄酸受体，包括视黄酸受体α（RAR alpha），RAR beta，RXR beta和RXR gamma，均在Apc（Min / +）腺瘤中表达。此外，我们的结果表明，RXRα下调是大肠癌发生的早期事件，并且独立于β-catenin表达。 GT显着增加了RXRα的蛋白质水平。此外，RT-PCR分析表明，GT诱导了RXRαmRNA水平的类似增加。结肠DNA的基因组亚硫酸氢盐处理，然后RXR alpha基因启动子区域中24个CpG位点的焦磷酸测序显示，GT处理可显着降低CpG甲基化。结果表明，低浓度的GT足以使RXRα沉默并抑制Apc（Min / +）小鼠的肠道肿瘤发生。

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