Yonago Acta medica 1996;38:221-228

Growth Suppression Function of the Human Glioblastoma Cell Line, T98G via Microcell-Mediated Transfer of Chromosome 17

Hideki Kamitani, Izumi Horikawa*, Tomokatsu Hori and Mitsuo Oshimura*

Division of Neuosurgery, Institute of Neurological Sciences and *Department of Molecular and Cell Genetics, Faculty of Medicine, Tottori University, Yonago 683, Japan

T98G cells were derived from a human glioblastoma multiforme tumor and they have mutant p53 alleles without the wild type. To examine the phenotypic alterations caused by correcting the defect, we introduced a single human chromosome 17 tagged with the pSV2neo gene into the T98G cells via microcell fusion. Although G-418-resistant colonies were obtained, the short arm p53 locus of the transferred chromosome 17 was commonly lost as demonstrated by means of Southern blotting with restriction fragment length polymorphism or variable number of tandem repeat markers of chromosome 17. These clones did not have an altered cell morphology or in vitro growth properties, including a population doubling time, saturation density and serum-independent growth. The findings suggest that the cells with the intact chromosome 17 underwent growth inhibition or arrest at an early stage and revertants with loss of the wild type p53 appeared, indicating that one copy of the p53 gene is sufficient to exert a growth inhibitory effect under physiological conditions.

Key words: chromosome 17; chromosome transfer; glioblastoma; growth suppression; p53

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