Sansom Owen J, Berger Jennifer, Bishop Stefan M, Hendrich Brian, Bird Adrian, Clarke Alan R
Cardiff School of Biosciences, Cardiff University, Cardiff, Wales, UK.
Nat Genet. 2003 Jun;34(2):145-7. doi: 10.1038/ng1155.
Gene silencing through de novo methylation of CpG island promoters contributes to cancer. We find that Mbd2, which recruits co-repressor complexes to methylated DNA, is essential for efficient tumorigenesis in the mouse intestine. As Mbd2-deficient mice are viable and fertile, their resistance to intestinal cancer may be of therapeutic relevance.
通过CpG岛启动子的从头甲基化实现的基因沉默与癌症相关。我们发现,Mbd2可将共抑制复合物招募至甲基化DNA,它对于小鼠肠道的高效肿瘤发生至关重要。由于Mbd2基因缺陷的小鼠能够存活且可育,它们对肠道癌症的抗性可能具有治疗意义。