作者: Xin Gui , Haiyan Li , Tianming Li , Hu Pu , Dongdong Lu
DOI: 10.1038/MT.2015.166
关键词:
摘要: Long noncoding RNA cancer upregulated drug resistant (CUDR) is overexpressed in many tumors and promotes tumorigenesis. Herein, we demonstrate CUDR could enhance the human embryonic stem cells (ESC) differentiation into hepatocyte-like by reducing trimethylation on histone H3 twenty-seventh lysine (H3K27me3). On other hand, excessive triggers malignant transformation. Mechanistically, identify causes highly liver (HULC) β-catenin abnormal expression inhibiting HULC promoter methylation promoting promoter-enhancer chromatin looping formation mediated CUDR-ccctc-binding factor (CTCF) complex, which recruits more polII P300. Strikingly, activity are crucial for oncogenic function. These findings provide first demonstration that plays a positive potential role cell through cascade of CUDR-HULC/CUDR-β-catenin signaling, offer insights novel link between long (lncRNA) epigenetic modification cells.