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Publication : CREPT accelerates tumorigenesis by regulating the transcription of cell-cycle-related genes.

First Author  Lu D Year  2012
Journal  Cancer Cell Volume  21
Issue  1 Pages  92-104
PubMed ID  22264791 Mgi Jnum  J:180279
Mgi Id  MGI:5306054 Doi  10.1016/j.ccr.2011.12.016
Citation  Lu D, et al. (2012) CREPT Accelerates Tumorigenesis by Regulating the Transcription of Cell-Cycle-Related Genes. Cancer Cell 21(1):92-104
abstractText  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 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.
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