Epigenetic disruption of cell signaling in nasopharyngeal carcinoma.
- Author:
Li-Li LI
1
;
Xing-Sheng SHU
;
Zhao-Hui WANG
;
Ya CAO
;
Qian TAO
Author Information
1. Shenzhen Key Laboratory of Cancer Nanotechnology, Institute of Biomedical and Health Engineering, Shenzhen Institutes of Advanced Technology, Chinese Academy of Sciences-CUHK, Shenzhen, Guangdong 518055, P. R. China.
- Publication Type:Journal Article
- MeSH:
Adaptor Proteins, Signal Transducing;
genetics;
metabolism;
Apoptosis;
genetics;
Carcinoma;
Cell Cycle;
genetics;
CpG Islands;
genetics;
DNA Damage;
genetics;
DNA Methylation;
Epigenesis, Genetic;
GTP Phosphohydrolases;
genetics;
metabolism;
Gene Silencing;
Humans;
Nasopharyngeal Neoplasms;
genetics;
metabolism;
pathology;
Repressor Proteins;
genetics;
metabolism;
Signal Transduction;
Tumor Suppressor Protein p53;
genetics;
metabolism;
beta Catenin;
genetics;
metabolism;
ras Proteins;
genetics;
metabolism;
rho GTP-Binding Proteins;
genetics;
metabolism
- From:Chinese Journal of Cancer
2011;30(4):231-239
- CountryChina
- Language:English
-
Abstract:
Nasopharyngeal carcinoma (NPC) is a malignancy with remarkable ethnic and geographic distribution in southern China and Southeast Asia. Alternative to genetic changes, aberrant epigenetic events disrupt multiple genes involved in cell signaling pathways through DNA methylation of promoter CpG islands and/or histone modifications. These epigenetic alterations grant cell growth advantage and contribute to the initiation and progression of NPC. In this review, we summarize the epigenetic deregulation of cell signaling in NPC tumorigenesis and highlight the importance of identifying epigenetic cell signaling regulators in NPC research. Developing pharmacologic strategies to reverse the epigenetic-silencing of cell signaling regulators might thus be useful to NPC prevention and therapy.
