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本文引用的文献

1
EZH2 promotes malignant behaviors via cell cycle dysregulation and its mRNA level associates with prognosis of patient with non-small cell lung cancer.EZH2 通过细胞周期失调促进恶性行为,其 mRNA 水平与非小细胞肺癌患者的预后相关。
PLoS One. 2012;7(12):e52984. doi: 10.1371/journal.pone.0052984. Epub 2012 Dec 31.
2
Global DNA hypomethylation in cancer: review of validated methods and clinical significance.癌症中的全球 DNA 低甲基化:已验证方法和临床意义的综述。
Clin Chem Lab Med. 2012 Oct 1;50(10):1733-42. doi: 10.1515/cclm-2011-0902.
3
A proteasome inhibitor-stimulated Nrf1 protein-dependent compensatory increase in proteasome subunit gene expression reduces polycomb group protein level.蛋白酶体抑制剂刺激的 Nrf1 蛋白依赖性代偿性增加蛋白酶体亚基基因表达,降低多梳蛋白组蛋白水平。
J Biol Chem. 2012 Oct 19;287(43):36179-89. doi: 10.1074/jbc.M112.359281. Epub 2012 Aug 29.
4
Polycomb protein EZH2 regulates tumor invasion via the transcriptional repression of the metastasis suppressor RKIP in breast and prostate cancer.多梳蛋白 EZH2 通过转录抑制乳腺癌和前列腺癌中的转移抑制因子 RKIP 来调节肿瘤侵袭。
Cancer Res. 2012 Jun 15;72(12):3091-104. doi: 10.1158/0008-5472.CAN-11-3546. Epub 2012 Apr 13.
5
Genetics and epigenetics of cutaneous malignant melanoma: a concert out of tune.皮肤恶性黑色素瘤的遗传学与表观遗传学:一曲失调的乐章
Biochim Biophys Acta. 2012 Aug;1826(1):89-102. doi: 10.1016/j.bbcan.2012.03.011. Epub 2012 Mar 31.
6
Sulforaphane induction of p21(Cip1) cyclin-dependent kinase inhibitor expression requires p53 and Sp1 transcription factors and is p53-dependent.翻译:萝卜硫素诱导 p21(Cip1)细胞周期蛋白依赖性激酶抑制剂表达需要 p53 和 Sp1 转录因子,并且依赖于 p53。
J Biol Chem. 2012 May 11;287(20):16168-78. doi: 10.1074/jbc.M111.305292. Epub 2012 Mar 15.
7
Promoter de-methylation of cyclin D2 by sulforaphane in prostate cancer cells.亚磺酰基丙烯酰胺促进前列腺癌细胞中环细胞 D2 的去甲基化。
Clin Epigenetics. 2011;3(1):3. doi: 10.1186/1868-7083-3-3. Epub 2011 Oct 26.
8
Sulforaphane suppresses polycomb group protein level via a proteasome-dependent mechanism in skin cancer cells.萝卜硫素通过蛋白酶体依赖性机制抑制皮肤癌细胞中的多梳蛋白水平。
Mol Pharmacol. 2011 Nov;80(5):870-8. doi: 10.1124/mol.111.072363. Epub 2011 Aug 1.
9
(-)-Epigallocatechin-3-gallate and DZNep reduce polycomb protein level via a proteasome-dependent mechanism in skin cancer cells.(-)-表没食子儿茶素没食子酸酯和 DZNep 通过蛋白酶体依赖性机制降低皮肤癌细胞中的多梳蛋白水平。
Carcinogenesis. 2011 Oct;32(10):1525-32. doi: 10.1093/carcin/bgr171. Epub 2011 Jul 27.
10
Histone deacetylase turnover and recovery in sulforaphane-treated colon cancer cells: competing actions of 14-3-3 and Pin1 in HDAC3/SMRT corepressor complex dissociation/reassembly.受硫代葡萄糖苷处理的结肠癌细胞中的组蛋白去乙酰化酶周转和恢复:14-3-3 和 Pin1 在 HDAC3/SMRT 共抑制复合物解离/组装中的竞争作用。
Mol Cancer. 2011 May 30;10:68. doi: 10.1186/1476-4598-10-68.

皮肤癌的表观遗传学癌症预防机制。

Epigenetic cancer prevention mechanisms in skin cancer.

机构信息

Departments of Biochemistry and Molecular Biology, University of Maryland School of Medicine, 108 N. Greene Street, Baltimore, Maryland, 21201, USA.

出版信息

AAPS J. 2013 Oct;15(4):1064-71. doi: 10.1208/s12248-013-9513-3. Epub 2013 Aug 1.

DOI:10.1208/s12248-013-9513-3
PMID:23904153
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3787232/
Abstract

Epigenetics is an important emerging area for study of mechanisms of cancer prevention. In recent years, it has been realized that cancer prevention agents, derived from natural dietary sources, impact cancer cell survival by modulating epigenetic processes. In the present manuscript, we review key epigenetic regulatory mechanisms and examine the impact of sulforaphane and green tea polyphenols on these processes. We also discuss available information on the epigenetics in the context of skin cancer. These studies indicate that diet-derived chemopreventive agents modulate DNA methylation status and histone modification via multiple processes and point to additional areas for study of epigenetic mechanisms in skin cancer.

摘要

表观遗传学是癌症预防机制研究的一个重要新兴领域。近年来,人们已经意识到,源自天然饮食来源的癌症预防剂通过调节表观遗传过程来影响癌细胞的存活。在本手稿中,我们回顾了关键的表观遗传调控机制,并研究了萝卜硫素和绿茶多酚对这些过程的影响。我们还讨论了有关皮肤癌表观遗传学的现有信息。这些研究表明,饮食来源的化学预防剂通过多种途径调节 DNA 甲基化状态和组蛋白修饰,并指出了皮肤癌中表观遗传机制研究的其他领域。