The transcriptional repression of the human Cu/Zn superoxide dismutase(sod1) gene by the anticancer drug, mitomycin C(MMC)

The Cu/Zn superoxide dismutase(sod1) is one of the key enzymes that protects cells against oxidative stress. In order to investigate the effects of mitomycin C(MMC) on the induction of apoptotic cell death and on the sod1 transcription level, the CATs activity of HepG2 cells transfected with sod1 pr...

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Bibliographic Details
Published in:Biochemistry and molecular biology international 1997-08, Vol.42 (5), p.949-956
Main Authors: Cho, G, Kang, S, Seo, S J, Kim, Y, Jung, G
Format: Article
Language:English
Subjects:
Antibiotics, Antineoplastic - pharmacology
Gene Expression Regulation, Neoplastic - drug effects
Humans
Mitomycins - pharmacology
Plasmids
Promoter Regions, Genetic
Superoxide Dismutase - biosynthesis
Superoxide Dismutase - genetics
Transcription, Genetic - drug effects
Transfection
Tumor Cells, Cultured
Tumor Suppressor Protein p53 - biosynthesis
Tumor Suppressor Protein p53 - genetics
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Summary:The Cu/Zn superoxide dismutase(sod1) is one of the key enzymes that protects cells against oxidative stress. In order to investigate the effects of mitomycin C(MMC) on the induction of apoptotic cell death and on the sod1 transcription level, the CATs activity of HepG2 cells transfected with sod1 promoter-CAT(chloramphenicol acetyl transferase) fusion reporter was measured after MMC treatment. The CAT assay showed that exposure of HepG2 cells to MMC decreased the transcription level of the sod1 gene. The accumulation of p53 tumor suppressor protein by MMC treatment of HepG2 cells was noted. In order to investigate the p53-negative response element in its promoter region, a p53 cotransfection experiment with serially deleted sod1 promoter/CAT reporter constructs was performed. The results show a significant reduction of CAT activity in all deletion reporter constructs. The results show that MMC treatment inhibited sod1 gene transcription through p53-mediated transcriptional repression.
ISSN:1039-9712