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Different G2/M accumulation in M059J and M059K cells after exposure to DNA double-strand break-inducing agents

Authors :
Juan Castro
Rolf Lewensohn
Thomas Heiden
Åsa Holgersson
Margareta Edgren
A. E. Meijer
Source :
International journal of radiation oncology, biology, physics. 61(3)
Publication Year :
2004

Abstract

Purpose To investigate and compare the cell cycle progression in relation to cell death in the human glioma cell lines, M059J and M059K, after exposure to DNA double-strand break–inducing agents. Methods and materials The M059J and M059K cells, deficient and proficient in the catalytic subunit of the DNA-dependent protein kinase, respectively, were exposed to 1 and 4 Gy of photons or accelerated nitrogen ions. In addition, M059J and M059K cells were treated with 10 and 40 μg/mL of bleomycin for 30 min, respectively. Cell cycle progression, monitored by DNA flow cytometry, was measured up to 72 h after treatment. Results M059J, but not M059K, cells displayed G 2 /M accumulation after low linear energy transfer irradiation. High linear energy transfer radiation exposure however, resulted in a substantial increase of M059K cells in the G 2 /M phase detected at 48 h. At 72 h, the number of cells in the G 2 /M phase was equivalent to its control. M059J cells accumulated mainly in S phase after high linear energy transfer irradiation. In contrast to M059K, M059J cells were still blocked at 72 h. Bleomycin induced G 2 /M accumulation for both M059J and M059K cells detected 24 h after treatment. At 48 h, the percentage of bleomycin-treated M059J cells in G 2 /M phase remained high, and the number of M059K cells had decreased to control levels. Neither cell line showed cell cycle arrest (≤10 h) after exposure to these agents. Conclusion Distinct cell cycle block and release is dependent on the complexity of the induced DNA damage and the presence of the DNA-dependent protein kinase catalytic subunit.

Details

ISSN :
03603016
Volume :
61
Issue :
3
Database :
OpenAIRE
Journal :
International journal of radiation oncology, biology, physics
Accession number :
edsair.doi.dedup.....739b06a3b69102e2eb0e78e29efec102