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Identification of proteins that regulate radiation-induced apoptosis in murine tumors with wild type p53
Jinsil Seong1, Hae Jin Oh, Jiyoung Kim
1Department of Radiation Oncology, Yonsei University Medical College, Seoul, Korea. jsseong@yumc.yonsei.ac.kr
Abstract:
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.
Insights
Radiation induces apoptosis differently in tumors with wild type p53. Proteomics revealed distinct molecular changes, suggesting cytochrome c oxidase and Nip 2 as potential targets for regulating tumor radiosensitivity.
Area of Science:
- Oncology
- Molecular Biology
- Radiotherapy Research
Background:
- Tumor radiosensitivity is crucial for effective radiation therapy.
- Wild type p53 is common in many tumors, yet radiosensitivity varies significantly.
- Understanding molecular determinants of apoptosis induction by radiation is essential.
Purpose of the Study:
- To investigate the molecular factors influencing radiation-induced apoptosis in murine tumors with wild type p53.
- To compare the proteomic profiles of radiosensitive and radioresistant tumors post-irradiation.
- To identify potential molecular targets for modulating tumor radiosensitivity.
Main Methods:
- Utilized two syngeneic murine tumors (OCa-I and HCa-I) with differing radiosensitivity but wild type p53.
- Irradiated tumors and collected samples at 4 hours post-irradiation for peak apoptosis analysis.
- Employed proteomics and peptide mass fingerprinting to identify differentially expressed proteins related to apoptosis.
Main Results:
- OCa-I tumors exhibited significantly higher radiosensitivity and apoptosis induction compared to HCa-I tumors.
- Radiation increased expression of cytochrome c oxidase and Nip 2 protein in OCa-I but not HCa-I.
- These proteins showed a >3-fold increase in the radiosensitive OCa-I tumors.
Conclusions:
- Radiosensitivity in tumors with wild type p53 is governed by complex molecular mechanisms.
- Cytochrome c oxidase and Nip 2 protein expression levels correlate with tumor radiosensitivity.
- These proteins represent potential therapeutic targets for enhancing radiosensitivity in cancer treatment.
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