Epigenetic mechanisms in senescence, immortalisation and cancer

被引:8
|
作者
Carnero, Amancio [1 ,2 ]
LLeonart, Matilde E. [3 ]
机构
[1] Hosp Univ Virgen Rocio, Inst Biomed Sevilla, Seville 41013, Spain
[2] CSIC, Seville 41013, Spain
[3] Hosp Valle De Hebron, Inst Recerca, Dept Pathol, Oncol & Pathol Grp, Barcelona 08035, Spain
关键词
methylation; epigenetic modifications; SAHH; senescence; immortalisation; cancer; MAMMARY EPITHELIAL-CELLS; TUMOR-SUPPRESSOR GENES; CPG ISLAND METHYLATION; REPEAT-CONTAINING RNA; DNA METHYLATION; CELLULAR SENESCENCE; HISTONE H3; PROMOTER HYPERMETHYLATION; TELOMERE-LENGTH; BREAST-CANCER;
D O I
10.1111/j.1469-185X.2010.00154.x
中图分类号
Q [生物科学];
学科分类号
07 ; 0710 ; 09 ;
摘要
Cancer is controlled not only by genetic events but also by epigenetic events. The active acquisition of epigenetic changes is a poorly understood but very important process in mammalian development, differentiation, and disease. It is well established that epigenetic events are controlled by a specific subgroup of proteins, such as DNA methyltransferases, histone acetylases histone lysine methyltransferases or histone deacetylases, that influence methylation or acetylation patterns to modulate gene expression. We and others have identified S-adenosylhomocysteine hydrolase in a high-throughput genetic screen focused on discovering novel genes whose inhibition induces immortalisation of primary cells. Herein, we address the importance of genes involved in epigenetic mechanisms during senescence and how their effects might determine senescence bypass and immortalisation. The ways in which genes that regulate epigenetic mechanisms might modulate senescence/immortalisation and how these pathways could influence cancer development are explored. Overall, epigenetic modifications seem to play a major role in cancer, influencing tumour outcome by interfering with key senescence pathways.
引用
收藏
页码:443 / 455
页数:13
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