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首页> 外文期刊>Journal of Cellular Physiology >Inhibition of PKC-Induced COX-2 and IL-8 Expression in Human Breast Cancer Cells by Glucosamine
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Inhibition of PKC-Induced COX-2 and IL-8 Expression in Human Breast Cancer Cells by Glucosamine

机译：抑制PKC-Induced cox - 2和引发在人类乳腺癌细胞表达葡萄糖胺

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摘要

Breast cancer is a common cancer leading to many deaths among females. Cyclooxygenase-2 (COX-2) and interleukin-8 (IL-8) are two highly expressed inflammatory mediators to be induced by the protein kinase C (PKC) signaling via various inflammatory stimuli and both contribute significantly to cancer metastasis/progression. Glucosamine has been shown to act as an anti-inflammation molecule. The aim of this study was to clarify the role and acting mechanism of glucosamine during the PKC-regulation of COX-2/IL-8 expression and the associated impact on breast cancer. In MCF-7 breast cancer cells, glucosamine effectively suppresses the PKC induction of COX-2 and IL-8 promoter activity, mRNA and protein levels, as well as the production of prostaglandin E-2 (PGE(2)) and IL-8. Glucosamine is able to promote COX-2 protein degradation in a calpain-dependent manner and IL-8 protein degradation in calpain-dependent and proteasome-dependent manners. The MAPK and NF-B pathways are involved in PKC-induced COX-2 expression, but only the NF-B pathway is involved in PKC-induced IL-8 expression. Glucosamine attenuates PKC-mediated IB phosphorylation, nuclear NF-B translocation, and NF-B reporter activation. Both PGE(2) and IL-8 promote cell proliferation and IL-8 induces cell migration; thus, glucosamine appears to suppress PKC-induced cell proliferation and migration. Furthermore, glucosamine significantly inhibits the growth of breast cancer xenografts and this is accompanied by a reduction in COX-2 and IL-8 expression. In conclusion, glucosamine seems to attenuate the inflammatory response in vitro and in vivo and this occurs, at least in part by targeting to the NF-B signaling pathway, resulting in an inhibition of breast cancer cell growth. J. Cell. Physiol. 230: 2240-2251, 2015. (c) 2015 Wiley Periodicals, Inc.
机译：乳腺癌是一种常见的癌症导致许多女性死亡。和interleukin-8(引发)是两个高度表达炎症介质诱导的通过各种蛋白激酶C (PKC)信号炎症刺激和贡献明显的癌症转移/发展。氨基葡萄糖作为一个已被证明抗炎分子。澄清的作用和作用机制葡萄糖胺PKC-regulation期间cox - 2 /引发表达和相关的影响在乳腺癌。葡萄糖胺有效地抑制PKC感应cox - 2和引发的推广活动,信使rna和蛋白质水平,以及生产前列腺素依照(铂族元素(2))引发。蛋白质降解calpain-dependent的方式并在calpain-dependent引发蛋白质降解和proteasome-dependent礼仪。NF-B通路参与PKC-induced cox - 2表达,但只有NF-B通路在PKC-induced引发表达式。变弱PKC-mediated IB磷酸化,核NF-B易位,NF-B记者激活。核扩散和引发诱发细胞迁移;因此,葡萄糖胺抑制PKC-induced出现细胞增殖和迁移。葡萄糖胺显著抑制的增长乳腺癌异种移植,这是陪同通过降低cox - 2和引发的表情。结论,葡萄糖胺似乎减弱了炎症反应在体外和体内这发生,至少在目标的一部分NF-B信号通路,导致一个抑制乳腺癌细胞的生长。杂志。230:2240 - 2251年,2015年。期刊、公司。

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