Mecp2-mediated Epigenetic Silencing of miR-137 Contributes to Colorectal Adenoma-Carcinoma Sequence and Tumor Progression via Relieving the Suppression of c-Met

• DOI: 10.1038/srep44543
• Publication Date: 2017-03-14T15:41:47Z
• Authors: Tao Chen; Shi-Lun Cai; Jian Li; Zhi-Peng Qi; Xu-Quan Li; Le-Chi Ye; Xiao-Feng Xie; Ying-Yong Hou; Li-Qing Yao; Mei-Dong Xu; Ping-Hong Zhou; Jian-Min Xu; Yun-Shi Zhong
• Keywords: MeCP2; Tumor progression

Abstract The molecular mechanisms underlying colorectal cancer (CRC) development remain elusive. In this study, we examined the miRNA and mRNA expressions in adenoma-carcinoma sequence (ACS), a critical neoplastic progression CRC development. We found that miR-137 was down-regulated all adenoma carcinoma tissues. Low levels were correlated negatively with tumor metastasis. Then identified inhibition effect of development, both cell lines mouse models. MiR-137 shown to control proliferation, colony formation, migration invasion growth further confirmed negative association between c-Met expression thus validated important oncogene as target CRC. addition, DNA methyl-CpG-binding protein, Mecp2, up-regulated ACS tissues via sequencing. Further experiment showed subjected epigenetic regulation mediated by Mecp2. also can be silencing suppressed coexpression Mecp2 miR-137. These findings highlight role miR-137-c-Met nexus reveal Mecp2-regulated silence causes downregulation carcinoma.