MiR-410 Is Overexpressed in Liver and Colorectal Tumors and Enhances Tumor Cell Growth by Silencing FHL1 via a Direct/Indirect Mechanism

• DOI: 10.1371/journal.pone.0108708
• Publication Date: 2014-10-01T13:56:24Z
• Authors: Yu Wang; Jie Fu; Mengmeng Jiang; Xiaoai Zhang; Long Cheng; Xiaojie Xu; Zhongyi Fan; Jing Zhang; Qinong Ye; Haifeng Song
• Keywords: Chromatin immunoprecipitation

FHL1 is an important tumor-suppressor that downregulated in multiple tumors by unknown mechanisms. We demonstrated miR-410 specifically targets the 3′UTR of FHL1. Furthermore, using DNA bisulfite modification and sequencing experiments, we promoter hypermethylated cancer cells. methylation increased upon expression, suggesting regulation occurs a dual mechanism. Using chromatin immunoprecipitation assays, observed overexpression results binding DNMT3A at promoter, which could explain how regulates methylation. Importantly, vitro vivo suggest may have oncogenic properties. both are upregulated clinical human liver colorectal cancers. Our function as oncomiR consistent with its key regulating certain digestive system