Epigenetic gene silencing in the Wnt pathway in breast cancer

被引:95
作者
Klarmann, George J. [1 ,2 ]
Decker, Amy [1 ,3 ]
Farrar, William L. [1 ]
机构
[1] NCI, Ctr Canc Res, Canc Stem Cell Stn, Lab Canc Prevent, Frederick, MD 21702 USA
[2] SAIC Frederick Inc, Frederick, MD USA
[3] Johns Hopkins Univ, Montgomery Cty Ctr, Biotechnol Program, Rockville, MD USA
关键词
breast cancer; DNA methylation; epigenetics; Wnt signaling; beta-catenin; cancer stem cell;
D O I
10.4161/epi.3.2.5899
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Breast cancer is one of the most common malignancies in women. Despite advances in treatment of endocrine-dependent tumors, the complete molecular basis of transformation is still unknown. What is clear is that a variety of genetic lesions and epigenetic modifications are present in the neoplasm. Disregulation of several signaling pathways is known to be associated with breast cancer development, among them is the wingless and integration site growth factor (Wnt) pathway. While genetic mutations of certain components of this pathway, such as APC, are significant contributing factors for colorectal cancers, they are typically not the predominate mechanism associated with breast cancer. Instead, it appears that DNA hypermethylation leads to aberrant regulation of the Wnt pathway in breast cancer, and as such, this review focuses on the epigenetic regulation of Wnt pathway components in breast cancer.
引用
收藏
页码:59 / 63
页数:5
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