Identification of Proteins that Regulate Radiation-induced Apoptosis in Murine Tumors with Wild Type p53

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  • SEONG Jinsil
    Department of Radiation Oncology, Yonsei University Medical College Brain Korea 21 Project for Medical Science, Yonsei University Medical College Institute for Gastroenterology, Yonsei University Medical College
  • OH Hae Jin
    Department of Radiation Oncology, Yonsei University Medical College Brain Korea 21 Project for Medical Science, Yonsei University Medical College
  • KIM Jiyoung
    Department of Radiation Oncology, Yonsei University Medical College Brain Korea 21 Project for Medical Science, Yonsei University Medical College
  • AN Jeung Hee
    Department of Radiation Oncology, Yonsei University Medical College Brain Korea 21 Project for Medical Science, Yonsei University Medical College
  • KIM Wonwoo
    Department of Radiation Oncology, Yonsei University Medical College Brain Korea 21 Project for Medical Science, Yonsei University Medical College

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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.<br> 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.<br>

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