The ERK1/2 pathway modulates nuclear PTEN-mediated cell cycle arrest by cyclin D1 transcriptional regulation

Hum Mol Genet. 2006 Sep 1;15(17):2553-9. doi: 10.1093/hmg/ddl177. Epub 2006 Jul 18.

Abstract

PTEN, a tumor suppressor phosphatase that dephosphorylates both protein and lipid substrates, is mutated in both heritable and sporadic breast cancer. Until recently, PTEN-mediated cell cycle arrest and apoptosis were thought to occur through its well-documented cytoplasmic activities. We have shown that PTEN localizes to the nucleus coincident with the G0-G1 phases of the cell cycle and that compartmentalization may regulate cell cycle progression dependent upon the down-regulation of cyclin D1. However, the mechanism for cyclin D1-dependent growth suppression by nuclear PTEN has remained largely undefined. Utilizing MCF-7 Tet-Off breast cancer cell lines stably expressing two different nuclear localization defective PTEN mutants, as well as wild-type PTEN and empty vector control cells, we demonstrate that nuclear PTEN down-regulates cyclin D1 transcription and this event is mediated by the down-regulation of MAPK specifically by nuclear localized PTEN. These results provide further evidence that nuclear PTEN plays a role through cell cycle suppression functions in regulating carcinogenesis.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cell Cycle
  • Cell Line, Tumor
  • Cell Nucleus / metabolism
  • Cyclin D1 / genetics*
  • Cyclin D1 / metabolism
  • Down-Regulation
  • Humans
  • Mitogen-Activated Protein Kinases / metabolism*
  • Nuclear Localization Signals / genetics
  • PTEN Phosphohydrolase / physiology*
  • Phosphorylation
  • Signal Transduction*
  • Suppression, Genetic*
  • Transcription, Genetic*
  • Transfection

Substances

  • Nuclear Localization Signals
  • Cyclin D1
  • Mitogen-Activated Protein Kinases
  • PTEN Phosphohydrolase
  • PTEN protein, human