Skip to main content
. 2015 Oct 13;23(12):1843–1853. doi: 10.1038/mt.2015.166

Figure 8.

Figure 8

Schematic diagram illustrating the mechanisms for excessive cancer upregulated drug-resistant (CUDR) promoting derived hepatocyte-like cells malignant transformation. CUDR could enhance the human embryonic stem cells differentiation into hepatocyte-like cell. On the other hand, excessive CUDR further triggers hepatocyte-like cells malignant transformation. Mechanistically, we reveal excessive CUDR causes highly upregulated in liver cancer (HULC) or β-catenin abnormal expression by inhibiting HULC promoter methylation, and promoting β-catenin promoter-enhancer chromatin DNA looping formation mediated by CUDR-CTCF complex, which recruits more RNA polII and P300. Thereby, HULC or β-catenin activity is crucial for CUDR oncogenic function.