Lin Z X, Chang C C, Trosko J E
Beijing Institute for Cancer Research, PRC.
Sci China B. 1990 Apr;33(4):435-43.
Gap junctional intercellular communication (GJIC) as measured by metabolic cooperation was examined in a rat glioma cell line P98F47. X-ray induced mutants of P98F47 cells were grown in 6-thioguanine selective medium (6TG medium) to separate 6TG-resistant HGPRT- mutant cells (6TGr). By co-culturing 200 6TGr cells with varied high densities of the wild type 6TG-sensitive cells (6TGs), it was found that the recovery of 6TGr cells depended on the density of 6TGs cells. Higher densities of 6TGs cells reduced the recovery of 6TGr cells. These results demonstrate the ability of P98F47 cells to perform metabolic cooperation which is indicative of GJIC. When metabolic cooperation was inhibited, increased recovery of 6TGr cells was observed. Presented results also demonstrate metabolic cooperation between P98F47 glioma cells and normal rat glial cells. Effect of tumor promoting chemicals on metabolic cooperation of P98F47 cells was studied. 3H-uridine nucleotide autoradiography technique was used to confirm the above observations. The results suggest that these cells may provide the basis for an in vitro assay specially to study brain tumor promoters and neurotoxins.
通过代谢合作来测定的间隙连接细胞间通讯(GJIC)在大鼠胶质瘤细胞系P98F47中进行了检测。P98F47细胞经X射线诱导的突变体在6-硫鸟嘌呤选择性培养基(6TG培养基)中培养,以分离出对6TG耐药的次黄嘌呤-鸟嘌呤磷酸核糖转移酶突变细胞(6TGr)。通过将200个6TGr细胞与不同高密度的野生型6TG敏感细胞(6TGs)共培养,发现6TGr细胞的恢复取决于6TGs细胞的密度。更高密度的6TGs细胞降低了6TGr细胞的恢复率。这些结果证明了P98F47细胞进行代谢合作的能力,这表明存在GJIC。当代谢合作受到抑制时,观察到6TGr细胞的恢复增加。所呈现的结果还证明了P98F47胶质瘤细胞与正常大鼠神经胶质细胞之间的代谢合作。研究了肿瘤促进化学物质对P98F47细胞代谢合作的影响。使用3H-尿苷核苷酸放射自显影技术来证实上述观察结果。结果表明,这些细胞可能为专门研究脑肿瘤启动子和神经毒素的体外试验提供基础。