YY1 promotes colorectal cancer proliferation through the /E2F1 axis.

We previously reported that E2F1 expression is up-regulated and positively correlated with the malignant phenotypes of colorectal cancer (CRC). However, the underlying mechanisms leading to the aberrant up-regulation of E2F1 in CRC have not been clarified. In this study, we observed that directly targets the 3'UTR of mRNA, leading to reduced E2F1 expression. Overexpression of inhibited the proliferation of CRC cells by decreasing the level of E2F1. We also found that the Ying Yang 1 (YY1)-dependent transcriptional suppression of is responsible for the up-regulation of E2F1 in CRC, in which YY1 binds to the promoter of gene and recruits histone deacetylase (HDAC). Knockdown of YY1 led to cell cycle arrest and diminished colony formation in CRC cells partly through relieving the suppression. Clinical analysis showed that YY1 and E2F1 were negatively correlated with in CRC tissues. Moreover, a high level of YY1 and E2F1, or a low level of , predicted poor survival of CRC patients. In conclusion, our findings highlight the dysregulation of the YY1//E2F1 axis in CRC development, implicating a novel regulatory pathway for E2F1 as a potential therapeutic target in CRC.