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  • 标题:Identification of Proteins that Regulate Radiation-induced Apoptosis in Murine Tumors with Wild Type p53
  • 其他标题:Identification of Proteins that Regulate Radiation-induced Apoptosis in Murine Tumors with Wild Type p53
  • 本地全文:下载
  • 作者:Jinsil SEONG ; Hae Jin OH ; Jiyoung KIM
  • 期刊名称:Journal of Radiation Research
  • 印刷版ISSN:0449-3060
  • 电子版ISSN:1349-9157
  • 出版年度:2007
  • 卷号:48
  • 期号:5
  • 页码:435-441
  • DOI:10.1269/jrr.07015
  • 摘要:In this study, we investigated the molecular factors determining the induction of apoptosis by radiation. Two murine tumors syngeneic to C3H/HeJ mice were used: an ovarian carcinoma OCa-I, and a hepatocarcinoma HCa-I. Both have wild type p53, but display distinctly different radiosensitivity in terms of specific growth delay (12.7 d in OCa-I and 0.3 d in HCa-I) and tumor cure dose 50% (52.6 Gy in OCa-I and > 80 Gy in HCa-I). Eight-mm tumors on the thighs of mice were irradiated with 25 Gy and tumor samples were collected at regular time intervals after irradiation. The peak levels of apoptosis were 16.1 ± 0.6% in OCa-I and 0.2 ± 0.0% in HCa-I at 4 h after radiation, and this time point was used for subsequent proteomics analysis. Protein spots were identified by peptide mass fingerprinting with a focus on those related to apoptosis. In OCa-I tumors, radiation increased the expression of cytochrome c oxidase and Bcl2/adenovirus E1B-interacting 2 (Nip 2) protein higher than 3-fold. However in HCa-I, these two proteins showed no significant change. The results suggest that radiosensitivity in tumors with wild type p53 is regulated by a complex mechanism. Furthermore, these proteins could be molecular targets for a novel therapeutic strategy involving the regulation of radiosensitivity.
  • 关键词:Radiosensitivity; Apoptosis; Murine tumor; Proteomics
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