Tumorigenesis is closely associated with genetic altera- tions and epigenetic modifications (3). Epigenetic modification results from promoter methylation and/or alterations in histone modification in cancer cells (4). DNA methylation and histone modifications are interlinked via methyl-CpG-binding

Methyl-CpG-binding protein 2 (MeCP2) is a transcriptional repressor that has been implicated in tumor onset and progression. Compared with normal and other tumorous tissue, MeCP2 is highly expressed in well-differentiated adenocarcinoma and mucinous adenocarcinoma tissues, particularly at the invasion site of colorectal cancer tissues. The aim of the present study was to evaluate the potential of MeCP2 for use as a therapeutic target for human colorectal cancer. The DLD-1 colorectal cancer cell line was subjected to lentivirus-mediated short hairpin RNA-induced knockdown of MeCP2 and the effects on cell growth, cell cycle progression and cell migration were assessed. It was confirmed that lentivirus‐mediated RNA interference successfully suppressed MeCP2 expression in vitro, which was demonstrated to result in reduced cell viability, cell cycle arrest in G0/G1 phase and inhibition of cell migration. These results indicated that MeCP2 may serve as a potential target for gene therapy of colorectal cancer.