engleski

Constitutive expression and inducibility of plasminogen activator in Mer- glioblastoma A1235 cell line and in Mer+ A8 cells transfected with bacterial ada gene

The alkylation repair deficient (Mer- phenotype) cells produce higher levels of proteolytic enzyme plasminogen activator (PA) after treatment with alkylation agent N-methyl-N'-nitro-N-nitrosoguanidine (MNNG). The purpose of the present study was to investigate the induction and the stabilization of urokinase plasminogen activator (upa) transcripts in Mer- A1235 and in Mer+ A8 cells which harbor bacterial ada gene, following MNNG treatment. Northern blotting experiments revealed an increased amount of upa transcripts in Mer- A1235 human glioblastoma cell line treated with 5ƒÝM MNNG. However, no induction of upa transcript was detected in its Mer+ counterpart cells (A8 cells) following the same drug treatment. Studies with inhibitors of RNA and protein synthesis (actinomycin D and cycloheximide, respectively) indicate that the induced increase in amount of upa mRNA was due to enhanced transcription of the upa gene. Furthermore, they revealed that the turnover of the upa mRNA is relatively low (half-life, > 6 hr). These results demonstrate increase in transcription of upa gene in human glioblastoma Mer- cells after MNNG treatment. They suggest that induction of the upa gene might therefore be included in a cellular response to DNA damage.

A1235 human glioblastoma; Mer phenotype; MNNG; induction; urokinase plasminogen activator

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