[Abrogation effect of UCN-01 on radiation-induced G2 phase arrest of tumor cells and its mechanism]

Ai Zheng. 2005 Jan;24(1):1-6.
[Article in Chinese]

Abstract

Background & objective: Irradiation often causes cell cycle arrest in tumor cells. This study was to observe the abrogation of radiation-induced G(2) phase arrest of p53 mutated human cancer cell lines by 7-hydroxystaurosporine (UCN-01), and explore the mechanism.

Methods: Human nasopharyngeal carcinoma cell line CNE-1 and human lung adenocarcinoma cell line 973, both with p53 mutation, were used in this study. Human fibroblastoma cell line HT-1080 was used as control. Flow cytometry was used to observe the effects of irradiation on cell cycle of these 3 cell lines, and abrogation effect of UCN-01 on radiation-induced G(2) phase arrest. Western blot was used to detect phosphorylated CDC2-Tyr15 during the abrogation process.

Results: Irradiation resulted in G(2) phase arrest in CNE-1 cells and 973 cells. Proportion of cells in G(2) phase increased from 18.4% to 43.6% in CNE-1 cell line, and from 14.8% to 42.8% in 973 cell line after 2 Gy of irradiation. G(1) phase arrests, measured by "S phase cells consumption", of CNE-1 cells and 973 cells were much lower than that of HT-1080 cells (14.8% and -1.2% vs. 57.0%). Radiation-induced G(2) phase arrests were abrogated by UCN-01 from 63.5% to 16.1% in CNE-1 cell line, and from 35.4% to 16.3% in 973 cell line. UCN-01 suppressed the expression of radiation-induced phosphorylation of CDC2-Tyr15, which was in accordance with the abrogation of radiation-induced G(2) phase delay.

Conclusions: Main effect of irradiation on cell cycle of p53 mutated CNE-1 cells and 973 cells is G(2) phase arrest. UCN-01 is able to abrogate radiation-induced G(2) phase, which is associated with the reduction of phosphorylated CDC2-Tyr15.

Publication types

  • English Abstract
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adenocarcinoma / genetics
  • Adenocarcinoma / metabolism
  • Adenocarcinoma / pathology
  • Antineoplastic Agents / pharmacology
  • CDC2 Protein Kinase / metabolism*
  • Cell Line, Tumor
  • G2 Phase* / drug effects
  • G2 Phase* / radiation effects
  • Genes, p53
  • Humans
  • Lung Neoplasms / genetics
  • Lung Neoplasms / metabolism
  • Lung Neoplasms / pathology
  • Mutation
  • Nasopharyngeal Neoplasms / metabolism
  • Nasopharyngeal Neoplasms / pathology*
  • Particle Accelerators
  • Phosphorylation / drug effects
  • Protein Kinase C / antagonists & inhibitors
  • Protein Kinase Inhibitors / pharmacology
  • Staurosporine / analogs & derivatives*
  • Staurosporine / pharmacology

Substances

  • Antineoplastic Agents
  • Protein Kinase Inhibitors
  • 7-hydroxystaurosporine
  • Protein Kinase C
  • CDC2 Protein Kinase
  • Staurosporine