DNA damage-induced cell cycle checkpoints involve both p53-dependent and -independent pathways: role of telomere repeat binding factor 2

Br J Cancer. 2001 Sep 14;85(6):898-901. doi: 10.1054/bjoc.2001.2002.

Abstract

Treatment of colon cancer cells with MNNG causes DNA damage with reduced telomeric signals in a p53-dependent manner, but increased cell cycle arrest in S-G(2)/M by both p53-dependent and independent mechanisms. Results also indicate that cellular levels of TRF2 may play a critical role in MNNG-induced cell cycle arrest and apoptosis of colon cancer cells.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Apoptosis
  • Blotting, Western
  • Cell Cycle / drug effects*
  • Colonic Neoplasms / metabolism*
  • DNA / metabolism
  • DNA Damage*
  • DNA-Binding Proteins / metabolism*
  • Flow Cytometry
  • Humans
  • In Situ Hybridization, Fluorescence
  • Methylnitronitrosoguanidine / toxicity*
  • Polymerase Chain Reaction
  • Telomeric Repeat Binding Protein 2
  • Tumor Cells, Cultured / drug effects*
  • Tumor Suppressor Protein p53 / genetics
  • Tumor Suppressor Protein p53 / metabolism*

Substances

  • DNA-Binding Proteins
  • Telomeric Repeat Binding Protein 2
  • Tumor Suppressor Protein p53
  • Methylnitronitrosoguanidine
  • DNA