Oct-1 is involved in the transcriptional repression of the p15(INK4b) gene

FEBS Lett. 2007 Mar 20;581(6):1087-92. doi: 10.1016/j.febslet.2007.01.092. Epub 2007 Feb 14.

Abstract

p15(INK4b) functions as a tumor suppressor and implicated in cellular senescence. Here, we show that the Oct-1 binding site in the human p15(INK4b) gene promoter functions as a silencer. Oct-1 specifically interacts with this binding site in vitro and in vivo and SMRT and HDAC1 are present in the p15(INK4b) proximal promoter region. Moreover, mouse embryo fibroblasts (MEFs) lacking Oct-1 have shown significantly increased levels of p15(INK4b) protein compared to their normal counterparts. Treatment with a histone deacetylase (HDAC) inhibitor has activated the expression of p15(INK4b) in wild-type MEFs but has no effect in MEFs lacking Oct-1, suggesting that Oct-1 represses p15(INK4b) gene expression in an HDAC-dependent manner. Finally, we show that the expression of Oct-1 protein significantly decreases, whereas p15(INK4b) protein significantly increases with the cellular aging process. Taken together, these results suggest that Oct-1 is an important transcriptional repressor for p15(INK4b) gene and the transcriptional repression of the p15(INK4b) gene by Oct-1 may be one of the regulatory mechanisms of cellular senescence.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cell Line
  • Cellular Senescence / genetics
  • Cyclin-Dependent Kinase Inhibitor p15 / genetics*
  • Gene Expression Regulation / physiology
  • Humans
  • Octamer Transcription Factor-1 / physiology*
  • Repressor Proteins / physiology*
  • Transcription, Genetic*
  • Transfection

Substances

  • CDKN2B protein, human
  • Cyclin-Dependent Kinase Inhibitor p15
  • Octamer Transcription Factor-1
  • Repressor Proteins