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首页> 外文期刊>American Journal of Physiology >Activation of PPAR{gamma} by curcumin inhibits Moser cell growth and mediates suppression of gene expression of cyclin D1 and EGFR.
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Activation of PPAR{gamma} by curcumin inhibits Moser cell growth and mediates suppression of gene expression of cyclin D1 and EGFR.

机译：姜黄素对PPAR {γ}的激活抑制了Moser细胞的生长，并介导了细胞周期蛋白D1和EGFR基因表达的抑制。

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Colorectal cancer is a leading cause of cancer-related morbidity and mortality in the United States. Curcumin, the yellow pigment in turmeric, possesses inhibitory effects on growth of a variety of tumor cells by reducing cell proliferation and inducing apoptosis. Effects of the peroxisome proliferator-activated receptor-gamma (PPARgamma) on stimulating cell differentiation and on inducing cell cycle arrest have attracted attention from the perspective of treatment and prevention of cancer. The aim of this study was to elucidate the mechanisms by which curcumin inhibits colon cancer cell growth. In the present report, we observed that curcumin, in a dose-dependent manner, inhibited the growth of Moser cells, a human colon cancer-derived cell line, and stimulated the trans-activating activity of PPARgamma. Further studies demonstrated that activation of PPARgamma was required for curcumin to inhibit Moser cell growth. Activation of PPARgamma mediated curcumin suppression of the expression of cyclin D1, a critical protein in the cell cycle, in Moser cells. In addition, curcumin blocked EGF signaling by inhibiting EGF receptor (EGFR) tyrosine phosphorylation and suppressing the gene expression of EGFR mediated by activation of PPARgamma. In addition to curcumin reduction of the level of phosphorylated PPARgamma, inhibition of cyclin D1 expression played a major and significant role in curcumin stimulation of PPARgamma activity in Moser cells. Taken together, our results demonstrated for the first time that curcumin activation of PPARgamma inhibited Moser cell growth and mediated the suppression of the gene expression of cyclin D1 and EGFR. These results provided a novel insight into the roles and mechanisms of curcumin in inhibition of colon cancer cell growth and potential therapeutic strategies for treatment of colon cancer.
机译：在美国，结直肠癌是与癌症相关的发病率和死亡率的主要原因。姜黄素是姜黄中的黄色素，通过减少细胞增殖和诱导细胞凋亡，对多种肿瘤细胞的生长具有抑制作用。从癌症的治疗和预防的角度来看，过氧化物酶体增殖物激活受体-γ（PPARγ）对刺激细胞分化和诱导细胞周期停滞的影响已引起关注。这项研究的目的是阐明姜黄素抑制结肠癌细胞生长的机制。在本报告中，我们观察到姜黄素以剂量依赖性方式抑制人结肠癌衍生的细胞系Moser细胞的生长，并刺激PPARγ的反式激活活性。进一步的研究表明姜黄素抑制Moser细胞生长需要激活PPARγ。在Moser细胞中，PPARγ介导的姜黄素激活可抑制细胞周期蛋白D1（细胞周期中的关键蛋白）的表达。此外，姜黄素通过抑制EGF受体（EGFR）酪氨酸磷酸化和抑制PPARgamma激活介导的EGFR基因表达来阻断EGF信号传导。除了姜黄素降低磷酸化的PPARgamma的水平外，抑制细胞周期蛋白D1的表达在姜黄素刺激Moser细胞中PPARgamma活性中也起着重要的作用。两者合计，我们的结果首次证明姜黄素激活PPARgamma抑制Moser细胞生长并介导细胞周期蛋白D1和EGFR基因表达的抑制。这些结果为姜黄素在抑制结肠癌细胞生长中的作用和机制以及潜在的结肠癌治疗策略提供了新颖的见解。

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