Epigenetic disruption of cell signaling in nasopharyngeal carcinoma

Chin J Cancer. 2011 Apr;30(4):231-9. doi: 10.5732/cjc.011.10080.

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.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Adaptor Proteins, Signal Transducing / genetics
  • Adaptor Proteins, Signal Transducing / metabolism
  • Apoptosis / genetics
  • Carcinoma
  • Cell Cycle / genetics
  • CpG Islands / genetics*
  • DNA Damage / genetics
  • DNA Methylation*
  • Epigenesis, Genetic*
  • GTP Phosphohydrolases / genetics
  • GTP Phosphohydrolases / metabolism
  • Gene Silencing
  • Humans
  • Nasopharyngeal Carcinoma
  • Nasopharyngeal Neoplasms / genetics*
  • Nasopharyngeal Neoplasms / metabolism
  • Nasopharyngeal Neoplasms / pathology
  • Repressor Proteins / genetics
  • Repressor Proteins / metabolism
  • Signal Transduction*
  • Tumor Suppressor Protein p53 / genetics
  • Tumor Suppressor Protein p53 / metabolism
  • beta Catenin / genetics
  • beta Catenin / metabolism
  • ras Proteins / genetics
  • ras Proteins / metabolism
  • rho GTP-Binding Proteins / genetics
  • rho GTP-Binding Proteins / metabolism

Substances

  • Adaptor Proteins, Signal Transducing
  • Repressor Proteins
  • Tumor Suppressor Protein p53
  • WIF1 protein, human
  • beta Catenin
  • GTP Phosphohydrolases
  • ras Proteins
  • rho GTP-Binding Proteins