Epigenetic "bivalently marked" process of cancer stem cell-driven tumorigenesis

被引：29

作者：

Balch, Curt

Nephew, Kenneth P.

Huang, Tim H. -M.

Bapat, Sharmila A. ^{[1
]}

机构：

[1] Natl Ctr Cell Sci, NCCS Complex, Pune 411007, Maharashtra, India

[2] Indiana Univ, Med Sci Program, Bloomington, IN USA

[3] Indiana Univ, Ctr Canc, Indianapolis, IN 46204 USA

[4] Ohio State Univ, Ctr Comprehens Canc, Human Canc Genet Program, Columbus, OH 43210 USA

来源：

BIOESSAYS | 2007年 / 29卷 / 09期

关键词：

TUMOR-SUPPRESSOR GENES; POLYCOMB; DIFFERENTIATION; IDENTIFICATION; 5-AZACYTIDINE; MECHANISMS; CONTRIBUTE; REVERSES; THERAPY; RENEWAL;

D O I：

10.1002/bies.20619

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：

Silencing of tumor suppressor genes (TSGs), by DNA methylation, is well known in adult cancers. However, based on the "stem cell" theory of tumorigenesis, the early epigenetic events arising in malignant precursors remain unknown. A recent report((1)) demonstrates that, while pluripotent embryonic stem cells lack DNA methylation and possess a "bivalent" pattern of activating and repressive histone marks in numerous TSGs, analogous multipotent malignant cells derived from germ cell tumors (embryonic carcinoma cells) gain additional silencing modifications to those same genes. These results suggest a possible mechanism by which aberrant differentiation, mediated by histone and DNA methylation, instigates tumor progression.

引用

页码：842 / 845

页数：4

共 30 条

[1] Dominant-negative histone H3 lysine 27 mutant derepresses silenced tumor suppressor genes and reverses the drug-resistant phenotype in cancer cells [J].