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

Cancer Cell. 2012 Jan 17;21(1):92-104. doi: 10.1016/j.ccr.2011.12.016.


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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cell Cycle / genetics
  • Cell Cycle Proteins / genetics
  • Cell Cycle Proteins / metabolism
  • Cell Cycle Proteins / physiology*
  • Cell Line, Tumor
  • Cell Proliferation
  • Cell Transformation, Neoplastic / genetics*
  • Cell Transformation, Neoplastic / metabolism
  • Embryonic Development / genetics
  • Gene Expression Regulation, Neoplastic*
  • Genes, bcl-1 / genetics
  • Humans
  • Mice
  • Molecular Sequence Data
  • Neoplasm Proteins / genetics
  • Neoplasm Proteins / metabolism
  • Neoplasm Proteins / physiology*
  • Neoplasms / genetics
  • Neoplasms / metabolism
  • Protein Interaction Mapping
  • RNA Polymerase II / metabolism
  • RNA, Messenger / metabolism
  • Transcription, Genetic


  • CREPT protein, mouse
  • Cell Cycle Proteins
  • Neoplasm Proteins
  • RNA, Messenger
  • RPRD1B protein, human
  • RNA Polymerase II

Associated data

  • GENBANK/DQ372930
  • GENBANK/DQ372938
  • GENBANK/DQ372939