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金松双黄酮对人乳腺癌细胞系MCF-7中胰岛素样生长因子-1刺激的细胞周期进程的影响。

Effects of Auraptene on IGF-1 Stimulated Cell Cycle Progression in the Human Breast Cancer Cell Line, MCF-7.

作者信息

Krishnan Prasad, Kleiner-Hancock Heather

机构信息

Department of Pharmacology, Toxicology & Neuroscience, Louisiana State University, Health Sciences Center, 1501 Kings Highway, Shreveport, LA 71130, USA ; Department of Veterinary and Biomedical Sciences, Center for Molecular Toxicology and Carcinogenesis, Pennsylvania State University, University Park, PA 16802, USA.

出版信息

Int J Breast Cancer. 2012;2012:502092. doi: 10.1155/2012/502092. Epub 2012 Dec 18.

DOI:10.1155/2012/502092
PMID:23320178
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3536038/
Abstract

Auraptene is being investigated for its chemopreventive effects in many models of cancer including skin, colon, prostate, and breast. Many mechanisms of action including anti-inflammatory, antiproliferative, and antiapoptotic effects are being suggested for the chemopreventive properties of auraptene. We have previously shown in the N-methylnitrosourea induced mammary carcinogenesis model that dietary auraptene (500 ppm) significantly delayed tumor latency. The delay in time to tumor corresponded with a significant reduction in cyclin D1 protein expression in the tumors. Since cyclin D1 is a major regulator of cell cycle, we further studied the effects of auraptene on cell cycle and the genes related to cell cycle in MCF-7 cells. Here we show that auraptene significantly inhibited IGF-1 stimulated S phase of cell cycle in MCF-7 cells and significantly changed the transcription of many genes involved in cell cycle.

摘要

金柑黄酮正在多种癌症模型(包括皮肤癌、结肠癌、前列腺癌和乳腺癌)中接受化学预防作用的研究。对于金柑黄酮的化学预防特性,人们提出了多种作用机制,包括抗炎、抗增殖和抗凋亡作用。我们之前在N-甲基亚硝基脲诱导的乳腺癌发生模型中表明,饮食中的金柑黄酮(500 ppm)显著延迟了肿瘤潜伏期。肿瘤发生时间的延迟与肿瘤中细胞周期蛋白D1蛋白表达的显著降低相对应。由于细胞周期蛋白D1是细胞周期的主要调节因子,我们进一步研究了金柑黄酮对MCF-7细胞中细胞周期以及与细胞周期相关基因的影响。在此我们表明,金柑黄酮显著抑制了MCF-7细胞中IGF-1刺激的细胞周期S期,并显著改变了许多参与细胞周期的基因的转录。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c998/3536038/aa95887e6708/IJBC2012-502092.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c998/3536038/88cb531773fd/IJBC2012-502092.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c998/3536038/aa95887e6708/IJBC2012-502092.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c998/3536038/88cb531773fd/IJBC2012-502092.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c998/3536038/aa95887e6708/IJBC2012-502092.002.jpg

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Sustained c-Jun-NH2-kinase activity promotes epithelial-mesenchymal transition, invasion, and survival of breast cancer cells by regulating extracellular signal-regulated kinase activation.
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