Wang X, Iliakis G
Thomas Jefferson University, Department of Radiation, Oncology and Nuclear Medicine, Philadelphia, PA 19107.
Int J Radiat Biol. 1993 Aug;64(2):165-8. doi: 10.1080/09553009314551251.
We have previously shown that two cell lines, 2.8 and 3.7, obtained from rat embryo fibroblasts (REF) by transfection with the oncogenes, H-ras plus v-myc, experience a prolonged inhibition of DNA replication after exposure to ionizing radiation as compared with normal REF, or REF expressing, H-ras or v-myc alone. We report here that four additional cell lines generated in our laboratory by cotransfection of REF with the same oncogenes also show prolonged inhibition of DNA replication after radiation exposure. These results indicate a regulatory mechanism for DNA replication in irradiated REF in which the products of the oncogenes H-ras and v-myc have a central role.
我们之前已经表明,通过用癌基因H-ras加v-myc转染从大鼠胚胎成纤维细胞(REF)获得的两个细胞系2.8和3.7,与正常REF或单独表达H-ras或v-myc的REF相比,在暴露于电离辐射后经历了DNA复制的长期抑制。我们在此报告,我们实验室通过用相同癌基因共转染REF产生的另外四个细胞系在辐射暴露后也显示出DNA复制的长期抑制。这些结果表明了受辐射REF中DNA复制的一种调节机制,其中癌基因H-ras和v-myc的产物起核心作用。