| Literature DB >> 26622593 |
L V Lv1, Jianyu Zhou2, Changwei Lin2, Gui Hu2, L U Yi3, Juan DU2, Kai Gao2, Xiaorong Li2.
Abstract
The dysregulation of microRNA (miRNA) expression is highly involved in cancer. Recently, a number of studies have demonstrated that the silencing of specific miRNAs is associated with DNA methylation. The muscle-specific miRNA-113b (miR-133b) is markedly downregulated in human colorectal cancer (CRC) compared with healthy colon cells, and is critical in the regulation of CRC cell proliferation and apoptosis. However, the mechanism of miR-133b downregulation in CRC has yet to be elucidated. Therefore, the aim of the present study was to determine the existence of an association between DNA methylation and miR-133b expression in CRC cells. It was identified that miR-133b promoter hypermethylation is upregulated in CRC tissues. To investigate the role of miR-133b methylation in CRC cells, the survival, cell cycle and invasion were analyzed in HT-29 and SW620 CRC cells treated with 5-aza-2'-deoxycytidine (5-Aza-CdR), 4-phenylbutyric acid (PBA) and 5-Aza-CdR/PBA. Functional analysis demonstrated that demethylation increased the expression of miR-133b, which restored migration and apoptosis in CRC cells. Thus, these results indicate that the regulation of miR-133b methylation may provide a novel therapeutic strategy for CRC treatment.Entities:
Keywords: DNA methylation; colorectal carcinoma; microRNA-133b
Year: 2015 PMID: 26622593 PMCID: PMC4509424 DOI: 10.3892/ol.2015.3336
Source DB: PubMed Journal: Oncol Lett ISSN: 1792-1074 Impact factor: 2.967