Enhanced G2-M Arrest by Nuclear Factor-κB-Dependent p21waf1/cip1 Induction

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Abstract

<jats:title>Abstract</jats:title> <jats:p>The transcription factor nuclear factor-κB (NF-κB) regulates cell survival pathways, but the molecular mechanisms involved are not completely understood. Here, we developed a NF-κB reporter cell system derived from CEM T leukemic cells to monitor the consequences of NF-κB activation following DNA damage insults. Cells that activated NF-κB in response to ionizing radiation or etoposide arrested in the G2-M phase for a prolonged time, which was followed by increased cell cycle reentry and survival. In contrast, those that failed to activate NF-κB underwent transient G2-M arrest and extensive cell death. Importantly, p21waf1/cip1 was induced in S-G2-M phases in a NF-κB-dependent manner, and RNA interference of this cell cycle regulator reduced the observed NF-κB-dependent phenotypes. Thus, cell cycle–coupled induction of p21waf1/cip1 by NF-κB represents a resistance mechanism in certain cancer cells.</jats:p>

Journal

  • Molecular Cancer Research

    Molecular Cancer Research 3 (6), 345-353, 2005-06-01

    American Association for Cancer Research (AACR)

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