Tumorigenesis is caused by an uncontrolled cell cycle and the altered expression of many genes. Here, we report a gene CREPT that is preferentially expressed in diverse human tumors. Overexpression of CREPTaccelerates tumor growth, whereas depletion of CREPTdemonstrates a reversed effect. CREPT regulates cyclin D1 expression by binding to its promoter, enhancing its transcription both in vivo and in vitro, and interacting with RNA polymerase II (RNAPII). Interestingly, CREPT promotes the formation of a chromatin loop and prevents RNAPII from reading through the 3' end termination site of the gene. Our findings reveal a mechanism where CREPT increases cyclin D1 transcription duringtumorigenesis, through enhancing the recruitment of RNAPII to the promoter region, possibly, as well as chromatin looping.

Lu DD, Wu YY, Wang YY, Ren FL, Wang DJ, Su FQ, Zhang YQ, Yang X, Jin GH, Hao XB, He DC, Zhai YG, Irwin DM, Hu J, Sung JJY, Yu J, Jia BQ*, Chang ZJ*. (2012) CREPT Accelerates Tumorigenesis by Regulating the Transcription of Cell-Cycle-Related Genes. Cancer Cell, 21(1):92-104.