Published online Jun 7, 2014. doi: 10.3748/wjg.v20.i21.6433
Revised: January 7, 2014
Accepted: February 17, 2014
Published online: June 7, 2014
Processing time: 186 Days and 17.5 Hours
Cancers, like other diseases, arise from gene mutations and/or altered gene expression, which eventually cause dysregulation of numerous proteins and noncoding RNAs. Changes in gene expression, i.e., upregulation of oncogenes and/or downregulation of tumor suppressor genes, can be generated not only by genetic and environmental factors but also by epigenetic factors, which are inheritable but nongenetic modifications of cellular chromosome components. Identification of the factors that contribute to individual cancers is a prerequisite to a full understanding of cancer mechanisms and the development of customized cancer therapies. The search for genetic and environmental factors has a long history in cancer research, but epigenetic factors only recently began to be associated with cancer formation, progression, and metastasis. Epigenetic alterations of chromatin include DNA methylation and histone modifications, which can affect gene-expression profiles. Recent studies have revealed diverse mechanisms by which chromatin modifiers, including writers, erasers and readers of the aforementioned modifications, contribute to the formation and progression of cancer. Furthermore, functional RNAs, such as microRNAs and long noncoding RNAs, have also been identified as key players in these processes. This review highlights recent findings concerning the epigenetic alterations associated with cancers, especially gastric cancer.
Core tip: The pathogenesis of gastric, or stomach cancer has long been a topic of extensive research, and these research efforts have resulted in tremendous improvements in the diagnosis and treatment of gastric cancer patients. However, research on gastric cancer has been focused on the genetic and environmental determinants of its formation and progression while the role of regulators, another important set of contributors to gastric cancer, has just begun to be elucidated. In this review, we highlight our current understanding of the epigenetic mechanisms by which gastric cancer arises and progresses and discuss future research directions.