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Identification of proteins that regulate radiation-induced apoptosis in murine tumors with wild type p53

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  More>>
Authors:
Seong, Jinsil; Oh, Hae Jin; Kim, Jiyoung; An, Jeung Hee; Kim, Wonwoo [1] 
  1. Dept. of Radiation Oncology, Yonsei Univ. Medical College, Seoul (Korea, Republic of)
Publication Date:
Sep 15, 2007
Product Type:
Journal Article
Resource Relation:
Journal Name: Journal of Radiation Research; Journal Volume: 48; Journal Issue: 5; Other Information: 32 refs., 4 figs., 2 tabs
Subject:
63 RADIATION, THERMAL, AND OTHER ENVIRONMENTAL POLLUTANT EFFECTS ON LIVING ORGANISMS AND BIOLOGICAL MATERIALS; ADENOVIRUS; APOPTOSIS; IRRADIATION; MICE; PROTEINS; RADIOSENSITIVITY; THERAPEUTIC USES; TIME-OF-FLIGHT MASS SPECTROMETERS; TUMOR CELLS; TWO-DIMENSIONAL ELECTROPHORESIS
OSTI ID:
20964791
Country of Origin:
Japan
Language:
English
Other Identifying Numbers:
Journal ID: ISSN 0449-3060; JRARAX; TRN: JP0704103113027
Submitting Site:
INIS
Size:
page(s) 435-441
Announcement Date:
Jan 07, 2008

Citation Formats

Seong, Jinsil, Oh, Hae Jin, Kim, Jiyoung, An, Jeung Hee, and Kim, Wonwoo. Identification of proteins that regulate radiation-induced apoptosis in murine tumors with wild type p53. Japan: N. p., 2007. Web. doi:10.1269/jrr.07015.
Seong, Jinsil, Oh, Hae Jin, Kim, Jiyoung, An, Jeung Hee, & Kim, Wonwoo. Identification of proteins that regulate radiation-induced apoptosis in murine tumors with wild type p53. Japan. https://doi.org/10.1269/jrr.07015
Seong, Jinsil, Oh, Hae Jin, Kim, Jiyoung, An, Jeung Hee, and Kim, Wonwoo. 2007. "Identification of proteins that regulate radiation-induced apoptosis in murine tumors with wild type p53." Japan. https://doi.org/10.1269/jrr.07015.
@misc{etde_20964791,
title = {Identification of proteins that regulate radiation-induced apoptosis in murine tumors with wild type p53}
author = {Seong, Jinsil, Oh, Hae Jin, Kim, Jiyoung, An, Jeung Hee, and Kim, Wonwoo}
abstractNote = {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. (author)}
doi = {10.1269/jrr.07015}
journal = []
issue = {5}
volume = {48}
place = {Japan}
year = {2007}
month = {Sep}
}