4.2 Review

Epigenetic Deregulations in Gastric Cancer

Journal

JOURNAL OF NANOSCIENCE AND NANOTECHNOLOGY
Volume 13, Issue 1, Pages 40-51

Publisher

AMER SCIENTIFIC PUBLISHERS
DOI: 10.1166/jnn.2013.6705

Keywords

Gastric Cancer (GC); Epigenetics; Hyper-Methylation; Histone Modification; MicroRNA

Funding

  1. National Key Program for Developing Basic Research [2010CB933903]
  2. NSFC [60927001, 60971045, 61271056, 21205013]
  3. Hunan Science and Technology Projects [2012SK3105, 2010sk2003]
  4. Scientific Research Fund of Hunan Provincial Education Department [11A030]

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Abnormal functioning of many cellular processes such as cell cycle, DNA repair, angiogenesis and cell-cell adhesion has been reported in all types of cancer. In the context of cancer, genes responsible to sustain integrity of the cells can be categorized into tumor suppressor genes and oncogenes. In normal conditions, these genes maintain a state of equilibrium and imbalance of these two groups of genes leads to a malignant form of cells known as Cancer. Genetics and epigenetics are the two main mechanisms that regulate expression of these genes. Silencing of tumor suppressor genes has been observed in different cancer while, on the other hand, silent oncogenes are active in cancer and confer growth advantage to malignant cells as compared with the contemporary normal cells. Gastric cancer (GC), like other cancers, is a complex disease. Multiple factors including bacterial infection, dietary habits, smoking and genetic polymorphisms determine the risk for GC development. Epigenetic modifications have been attributed as an initial event in the development of GC. Here, we have summarized recent findings in the field of epigenetics which correlated with GC.

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