PEG10 directly regulated by E2Fs might have a role in the development of hepatocellular carcinoma

AbstractPEG10 is an imprinted gene which is up-regulated in hepatocelluar carcinoma (HCC). However, the mechanism of PEG10 regulation remains to be elucidated. In this work the transcription factors E2F-1 and -4 were demonstrated to bind directly to the promoter of PEG10 and thereby regulate its expression. The expression profile of HCC tissues also suggested E2Fs were involved in PEG10 regulation. Further functional analysis showed that PEG10 was involved in the repression of apoptosis induced by serum deprivation and chemotherapeutic drugs. These findings link cancer genetics and epigenetics by showing that E2F acts directly upstream of an anti-apoptosis imprinted gene, PEG10

SVH-B interacts directly with p53 and suppresses the transcriptional activity of p53

AbstractWe previously reported that inhibition of SVH-B, a specific splicing variant of SVH, results in apoptotic cell death. In this study, we reveal that this apoptosis may be dependent on the presence of p53. Co-immunoprecipitation and GST pull-down assays have demonstrated that SVH-B directly interacts with p53. In both BEL-7404 cells and p53-null Saos-2 cells transfected with a temperature-sensitive mutant of p53, V143A, ectopically expressed SVH-B suppresses the transcriptional activity of p53, and suppression of SVH by RNA interference increases the transcriptional activity of p53. Our results suggested the function of SVH-B in accelerating growth and inhibition of apoptosis is related to its inhibitory binding to p53