| The C6-R cell line was derived from C6 glioma and exhibits key properties of radial glia. We analyzed the behavior of GFP labeled C6-R cells, C6R-G/H cells, in the intact and injured adult rat brain, and their influence on integration of neurons. At eleven days post-implantation, C6R-G/H cells were observed along the corpus callosum and hippocampus. PKH-26 labeled LGE embryonic neurons co-implanted with C6R-G/H cells co-migrated with them through a volume fourteen-fold the volume of neurons implanted alone. Controls with co-implantation of LGE embryonic neurons with fibroblasts yielded volumes somewhat greater than those obtained with neurons alone. In brains injured with ibotenic acid, the migration of C6R-G/H cells was more widespread and extended beyond the lesion cavity. When neurons were co-implanted with C6R-G/H cells they co-distributed beyond the lesion cavity, while neurons alone were found primarily in the cavity. The migratory properties of C6R-G/H cells and co-transplanted embryonic neurons suggest that C6R-G/H cells may serve as a scaffold or substrate for neuronal migration.; We investigated the capacity of C6R-G/H cells to generate tumors in the adult rat brain. Three weeks after implantation, all animals that received C6-G developed a high-grade glioma, while only 44% of animals implanted with C6R-G/H cells, developed tumors with maximal cross-sectional area 20-fold smaller, and with less malignant characteristics, such as angiogenesis and cell proliferation. Similar results were obtained in the brain of nude rats, suggesting no significant involvement of the immune system in suppressing growth of C6R-G/H cells.; Although the C6-R cell line resulted from transfection of C6 rat glioma cells with a construct encoding a mutant of RPTPβ, the encoded protein was not sufficient to account for the phenotypic differences between C6R-G/H and C6-G. Related clones expressing the same mutant protein were indistinguishable from C6 in morphology and tumorigenesis. While C6R-G/H cells, generated from transfection of C6-R cells with GFP-Hy, lack tumorigenicity, C6-R cells alone or transfected with either GFP or Hy plasmids alone still formed tumors, suggesting that the combination of GFP-Hy has a role in suppressing tumorigenesis. We suggest that the combination GFP-Hy may have a role in gene therapy for tumors. |
