Shay J W, Liu Y N, Werbin H
Department of Cell Biology, University of Texas Southwestern Medical Center, Dallas 75235.
Somat Cell Mol Genet. 1988 Jul;14(4):345-50. doi: 10.1007/BF01534642.
This report details studies of whether mouse NIH/3T3 TGr karyoplasts that are exposed to benzo[a]pyrene epoxide(trans) (BPDE) can progress to tumorigenicity when they are rescued with either mouse B10mtJ CAPr tumorigenic (experiment 1) or nontumorigenic (experiment 2) cytoplasts. The mitochondrial DNA of the B10mtJ cells has restriction fragment length differences that allow distinction from the mitochondrial DNA of the NIH/3T3 cells. The reconstructed clones in experiment 1 were all tumorigenic, while those from experiment 2 were all nontumorigenic. The clones in both experiments were passaged for an equivalent time. These findings reflect the presence of factors in mouse cytoplasm capable of suppressing the tumor phenotype of NIH/3T3-BPDE treated karyoplasts when rescued at an early stage of progression.
本报告详细介绍了关于暴露于苯并[a]芘环氧化物(反式)(BPDE)的小鼠NIH/3T3 TGr核质体,在用小鼠B10mtJ CAPr致瘤性(实验1)或非致瘤性(实验2)胞质体进行挽救时,是否能发展为致瘤性的研究。B10mtJ细胞的线粒体DNA具有限制性片段长度差异,这使得它能够与NIH/3T3细胞的线粒体DNA区分开来。实验1中的重建克隆均具有致瘤性,而实验2中的克隆均无致瘤性。两个实验中的克隆传代时间相同。这些发现反映了小鼠细胞质中存在一些因子,这些因子在进展早期进行挽救时能够抑制经BPDE处理的NIH/3T3核质体的肿瘤表型。