Histone H2AX sensitizes glioma cells to genotoxic stimuli by recruiting DNA double-strand break repair proteins

  • Authors:
    • Hiroyuki Momota
    • Shingo Ichimiya
    • Nobuhiko Kondo
    • Tomoki Kikuchi
    • Toshihiko Torigoe
    • Toshiaki Yamaki
    • Kiyohiro Houkin
    • Noriyuki Sato
  • View Affiliations

  • Published online on: August 1, 2003     https://doi.org/10.3892/ijo.23.2.311
  • Pages: 311-315
Metrics: Total Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )


Abstract

Glioblastoma is a life-threatening tumor in the human brain despite the fact that radio-chemotherapy inducing DNA damage has been improved in the last decade. Various studies focusing on the enhancement of the susceptibility of glioblastoma cells to DNA damage have been reported, which are aimed at more efficient treatment for the tumor. In this study, we show that radioresistant T98G glioblastoma cells can develop sensitivity to DNA damage induced by irradiation and etoposide as a result of the introduction of a DNA repair-associated histone, H2AX. Interestingly, when H2AX-transformed T98G cells were irradiated, Brca1 and Nbs1 were readily recruited in DNA double-strand break (DSB) foci and showed the G2/M-phase arrest of the cell cycle. Moreover, up-regulation of Brca1 was observed in H2AX-T98G cells after exposure to irradiation. Together with the evidence that H2AX transfection does not affect growth activities of non-tumor cells under genotoxic stimuli, this suggests that H2AX gene transfer would provide a new modality for radio-chemotherapy for glioblastomas, probably through overcoming the instability of the genome, and that Brca1 and Nbs1 might be crucial in this methodology.

Related Articles

Journal Cover

August 2003
Volume 23 Issue 2

Print ISSN: 1019-6439
Online ISSN:1791-2423

Sign up for eToc alerts

Recommend to Library

Copy and paste a formatted citation
x
Spandidos Publications style
Momota H, Ichimiya S, Kondo N, Kikuchi T, Torigoe T, Yamaki T, Houkin K and Sato N: Histone H2AX sensitizes glioma cells to genotoxic stimuli by recruiting DNA double-strand break repair proteins. Int J Oncol 23: 311-315, 2003
APA
Momota, H., Ichimiya, S., Kondo, N., Kikuchi, T., Torigoe, T., Yamaki, T. ... Sato, N. (2003). Histone H2AX sensitizes glioma cells to genotoxic stimuli by recruiting DNA double-strand break repair proteins. International Journal of Oncology, 23, 311-315. https://doi.org/10.3892/ijo.23.2.311
MLA
Momota, H., Ichimiya, S., Kondo, N., Kikuchi, T., Torigoe, T., Yamaki, T., Houkin, K., Sato, N."Histone H2AX sensitizes glioma cells to genotoxic stimuli by recruiting DNA double-strand break repair proteins". International Journal of Oncology 23.2 (2003): 311-315.
Chicago
Momota, H., Ichimiya, S., Kondo, N., Kikuchi, T., Torigoe, T., Yamaki, T., Houkin, K., Sato, N."Histone H2AX sensitizes glioma cells to genotoxic stimuli by recruiting DNA double-strand break repair proteins". International Journal of Oncology 23, no. 2 (2003): 311-315. https://doi.org/10.3892/ijo.23.2.311