Relationship of oncogene expression and radiosensitivity on mammalian cells.

本文用克隆形成法测定了5种小鼠肿瘤细胞系（FM 3A、3LL、EMT-6、FSa-II和SCC-VII）经Co-60 γ射线照射后的体外放射敏感性。EMT-6细胞耐药率最高。FM 3A、3LL和SCC-VII三种细胞系对FSa-II的敏感性相近，但均高于FSa-II细胞。用北方印迹杂交法检测c-myc和R-ras两种癌基因在体外培养细胞中的表达。c-myc基因在细胞中有表达，但c-myc mRNA水平与细胞的放射抗性无关。本研究中未检测到R-ras的表达。其他基因（Ha-ras、jun、raf等）的分析正在经历。在无血清培养基中用克隆形成试验检查正常和SV 40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角质形成细胞更敏感。野生型p53癌基因的表达，这可能会导致辐射后G1期阻滞，被抑制在转化细胞。因此，在转化细胞中，DNA损伤的修复可能受到抑制。本研究不能证实特定癌基因在细胞和肿瘤放射敏感性中的作用。野生型p53基因在肿瘤细胞中的作用有待进一步研究。

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.