Miyakoshi J, Kitagawa K, Yamagishi N, Ohtsu S, Day R S, Takebe H
Department of Radiation Genetics, Faculty of Medicine, Kyoto University, Sakyo-ku.
Jpn J Cancer Res. 1997 Jan;88(1):34-8. doi: 10.1111/j.1349-7006.1997.tb00298.x.
The A1235 and T98 cell lines derived from human gliomas have homozygous deletions in their p16 genes and are radiosensitive and radioresistant, respectively, with respect to other established glioma cell lines. These differences in radiosensitivity may be due to variations to some extent among cell lines, rather than genetically defined resistance or sensitivity. We examined the effect on radiation sensitivity of introducing a wild-type p16 gene into both p16-deficient glioma cell lines. The plasmid pOPMTS containing human wild-type p16 cDNA and a neomycin resistance gene, or the control plasmid pOPRSV1, were transfected into these cells. Clones from both cell lines, which expressed wild-type p16 mRNA constitutively after transfection with pOPMTS, were more radiosensitive than the parental cells and clones obtained after transfection with the negative control plasmid.
源自人类胶质瘤的A1235和T98细胞系在其p16基因中存在纯合缺失，相对于其他已建立的胶质瘤细胞系，它们分别对辐射敏感和抗辐射。这些辐射敏感性的差异可能在一定程度上是由于细胞系之间的差异，而不是基因定义的抗性或敏感性。我们研究了将野生型p16基因导入两种p16缺陷型胶质瘤细胞系对辐射敏感性的影响。将含有人类野生型p16 cDNA和新霉素抗性基因的质粒pOPMTS或对照质粒pOPRSV1转染到这些细胞中。用pOPMTS转染后持续表达野生型p16 mRNA的两种细胞系的克隆比亲代细胞和用阴性对照质粒转染后获得的克隆对辐射更敏感。
