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Relationship of oncogene expression and radiosensitivity on mammalian cells.

哺乳动物细胞癌基因表达与放射敏感性的关系。

基本信息

批准号：
04454297
负责人：
MORI Tomoyuki
金额：
$ 3.71万
依托单位：
Tokai University
依托单位国家：
日本
项目类别：
Grant-in-Aid for General Scientific Research (B)
财政年份：
1992
资助国家：
日本
起止时间：
1992 至 1994
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-04454297/
关键词：
Oncogene Radiosensitivity Tumor cells 放射線治療

项目摘要

Radiation sensitivity of five tumor cell lines (FM3A,3LL,EMT-6, FSa-II and SCC-VII) of mouse in vitro was examined with clonogenic assay after irradiation with Co-60 gamma-rays. EMT-6 cells were most resistant in these cell lines. Three cell lines (FM3A,3LL and SCC-VII) had the similar sensitivity and were more sensitive than FSa-II cells. Expression of two oncogenes, c-myc and R-ras, in cells in vitro was examined by northern blot hybridization analysis. Expression of c-myc gene was detected but the level of c-myc mRNA in cells did not correlate to the radioresistancy of cells. Expression of R-ras did not detected in the present study. Analysis of other genes (Ha-ras, jun, raf, etc.) is undergoing. Radiosensitivity of both normal and SV40-transformed keratinocytes was examined with clonogenic assay in a serum-free medium. Transformed keratinocytes was more sensitive than normal one. Expression of wild p53 oncogene, which may cause G1 arrest after irradiation, was inhibited in transformed cells. Therefore the repair of DNA damages may suppressed in transformed cells.The present study could not confirm the role of specific oncogene on radiosensitivity of cells and tumors. The role of wild p53 gene in rumor cells is remained to analyze.

以Co-60 γ射线辐照小鼠5种肿瘤细胞系（FM3A、3LL、EMT-6、FSa-II和SCC-VII）为研究对象，采用克隆致生实验检测其体外辐射敏感性。在这些细胞系中，EMT-6细胞的耐药性最强。FM3A、3LL和SCC-VII三种细胞系具有相似的敏感性，且敏感性高于FSa-II细胞。用northern blot杂交法检测细胞中c-myc和R-ras两种癌基因的表达。检测到c-myc基因的表达，但细胞中c-myc mRNA的表达水平与细胞的辐射抗性无关。本研究未检测到R-ras的表达。其他基因（Ha-ras, jun， raf等）的分析正在进行中。在无血清培养基中，用克隆实验检测正常和sv40转化的角质形成细胞的放射敏感性。转化角质形成细胞比正常细胞更敏感。照射后可能引起G1阻滞的野生p53癌基因的表达在转化细胞中被抑制。因此，在转化细胞中，DNA损伤的修复可能受到抑制。目前的研究还不能证实特异性癌基因对细胞和肿瘤放射敏感性的作用。野生p53基因在谣言细胞中的作用还有待分析。