Author/Authors :
Lu، نويسنده , , Dongdong and Wu، نويسنده , , Yinyuan and Wang، نويسنده , , Yinyin and Ren، نويسنده , , Fangli and Wang، نويسنده , , Dianjun and Su، نويسنده , , Fuqin and Zhang، نويسنده , , Yanquan and Yang، نويسنده , , Xi-lang Jin، نويسنده , , Guihua and Hao، نويسنده , , Xinbao and He، نويسنده , , Dacheng and Zhai، نويسنده , , Yonggong and Irwin، نويسنده , , David M. and Hu، نويسنده , , Jim and Sung، نويسنده , , Joseph J.Y. and Yu، نويسنده , , Jun-Ho Jia، نويسنده , , Baoqing and Chang، نويسنده , , Zhijie، نويسنده ,
Abstract :
Summary
genesis 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 CREPT accelerates tumor growth, whereas depletion of CREPT demonstrates 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 during tumorigenesis, through enhancing the recruitment of RNAPII to the promoter region, possibly, as well as chromatin looping.
