Open AccessTumor‐suppressive micro RNA silenced by tumor‐specific DNA hypermethylation in cancer cells
Author(s) -
Kozaki Kenichi,
Inazawa Johji
Publication year - 2012
Publication title -
cancer science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.035
H-Index - 141
eISSN - 1349-7006
pISSN - 1347-9032
DOI - 10.1111/j.1349-7006.2012.02236.x
Subject(s) - microrna , gene silencing , biology , gene , cpg site , dna methylation , intergenic region , non coding rna , rna , genetics , methylation , rna silencing , gene expression , cancer research , genome , rna interference
Micro RNA (mi RNA ) genes, located in intergenic or intragenic non‐coding regions of the genome, are transcribed and processed to small non‐protein‐coding RNA of approximately 22 nucleotides negatively regulating gene expression. Some mi RNA have already been reported for their genetic alterations, aberrant expression and oncogenic or tumor‐suppressive functions. After 2008, there has been a striking increase in the number of publications reporting tumor‐suppressive mi RNA ( TS ‐mi RNA ) silenced epigenetically in various types of cancers, suggesting important clinical applications for mi RNA ‐based molecular diagnosis and therapy for cancers. Here, we introduce a correlation of the gene silencing of TS ‐mi RNA through CpG island hypermethylation with the genomic distances between intergenic and intragenic mi RNA genes or protein‐coding host genes and CpG islands located around these genes. Furthermore, we also discuss the potential of mi RNA replacement therapy for cancers using double‐stranded RNA mimicking TS ‐mi RNA . ( Cancer Sci 2012; 103: 837–845)