Cancer Cell：“沉默”癌细胞基因新方法
美国科学家进行的一项最新研究发现，癌细胞内核小体（nucleosomes）密度的变化可以使这些细胞的基因沉默。这一研究成果有助科学家找到新的癌症治疗方法，相关论文发表在11月13日的《癌细胞》（Cancer Cell）杂志上。
（《癌细胞》（Cancer Cell），Vol 12, 432-444, 13 November 2007，Joy C. Lin, Peter A. Jones）
原始出处：
Cancer Cell, Vol 12, 432-444, 13 November 2007
Article
Role of Nucleosomal Occupancy in the Epigenetic Silencing of the MLH1 CpG Island
Joy C. Lin,1 Shinwu Jeong,1 Gangning Liang,1 Daiya Takai,1,2 Merhnaz Fatemi,1,3 Yvonne C. Tsai,1 Gerda Egger,1 Einav Nili Gal-Yam,1 and Peter A. Jones1,
1 Departments of Urology, Biochemistry, and Molecular Biology, Norris Comprehensive Cancer Center, Keck School of Medicine, University of Southern California, Los Angeles, Los Angeles, CA 90089, USA
Corresponding author
Peter A. Jones
jones_p@ccnt.usc.edu
Epigenetic silencing of tumor suppressor genes is generally thought to involve DNA cytosine methylation, covalent modifications of histones, and chromatin compaction. Here, we show that silencing of the three transcription start sites in the bidirectional MLH1 promoter CpG island in cancer cells involves distinct changes in nucleosomal occupancy. Three nucleosomes, almost completely absent from the start sites in normal cells, are present on the methylated and silenced promoter, suggesting that epigenetic silencing may be accomplished by the stable placement of nucleosomes into previously vacant positions. Activation of the promoter by demethylation with 5-aza-2′-deoxycytidine involves nucleosome eviction. Epigenetic silencing of tumor suppressor genes may involve heritable changes in nucleosome occupancy enabled by cytosine methylation.
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