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首页> 外文期刊>PPAR research >Fatty Acids of CLA-Enriched Egg Yolks Can Induce Transcriptional Activation of Peroxisome Proliferator-Activated Receptors in MCF-7 Breast Cancer Cells
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Fatty Acids of CLA-Enriched Egg Yolks Can Induce Transcriptional Activation of Peroxisome Proliferator-Activated Receptors in MCF-7 Breast Cancer Cells

机译:CLA富含蛋黄的脂肪酸可以诱导MCF-7乳腺癌细胞中过氧化物激素活化受体的转录激活

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摘要

In our previous study, we showed that fatty acids from CLA-enriched egg yolks (EFA-CLA) reduced the proliferation of breast cancer cells; however, the molecular mechanisms of their action remain unknown. In the current study, we used MCF-7 breast cancer cell line to determine the effect of EFA-CLA, as potential ligands for peroxisome proliferator-activated receptors (PPARs), on identified in silico PPAR-responsive genes: BCAR3, TCF20, WT1, ZNF621, and THRB (transcript TRβ2). Our results showed that EFA-CLA act as PPAR ligands with agonistic activity for all PPAR isoforms, with the highest specificity towards PPARγ. In conclusion, we propose that EFA-CLA-mediated regulation of PPAR-responsive genes is most likely facilitated by cis9,trans11CLA isomer incorporated in egg yolk. Notably, EFA-CLA activated PPAR more efficiently than nonenriched FA as well as synthetic CLA isomers. We also propose that this regulation, at least in part, can be responsible for the observed reduction in the proliferation of MCF-7 cells treated with EFA-CLA.
机译:在我们以前的研究中,我们表明来自CLA富含蛋黄(EFA-CLA)的脂肪酸降低了乳腺癌细胞的增殖;然而,其行动的分子机制仍然未知。在目前的研究中,我们使用MCF-7乳腺癌细胞系来确定EFA-CLA的效果,作为过氧化物组织增殖物激活的受体(PPAR)的潜在配体,在硅PPAR-响应基因中鉴定:BCAR3,TCF20,WT1 ,ZNF621和THRB(转录TRβ2)。我们的研究结果表明,EFA-CLA作为PPAR配体,具有对所有PPAR同种型的激动活性,对PPARγ的特异性具有最高的特异性。总之,我们提出,CIS9,CIS11CLA异构体最有可能促进EFA-CLA介导的PPAR-Chrenceive基因的调节。值得注意的是,EFA-CLA更有效地激活了PPAR而不是非成分的FA以及合成CLA异构体。我们还提出,至少部分地,该监管可负责观察到用EFA-CLA治疗的MCF-7细胞的增殖的降低。

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