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Immunolocalization and adenoviral vector-mediated manganese superoxide dismutase gene transfer to experimental oral
E W Lam1, H M Hammad, R Zwacka
1Department of Radiology, University of Iowa College of Medicine, Iowa City, USA. ernest.lam@ualberta.ca
Abstract:
The anti-oxidant enzyme system protects cellular macromolecules against damage from reactive oxygen species. One component of this system, manganese superoxide dismutase (MnSOD), has also been shown to display tumor suppressor gene-like activity. The purpose of this study was to examine changes in MnSOD expression during hamster cheek pouch carcinogenesis, and the effects of MnSOD overexpression using an adenoviral vector. Tumor induction was carried out using 7,12-dimethylbenz[alpha]anthracene. Animals were killed at periodic intervals, and cheek pouch tissues were excised and examined for MnSOD expression by immunohistochemistry and digital image analysis. We observed a reduction in MnSOD expression as early as 2 weeks after the start of carcinogen application. Low MnSOD expression persisted until the end of the 23-week experimental period. Solid hamster cheek pouch carcinoma xenografts were then established in nude mice. An adenoviral vector encoding the human MnSOD gene was delivered to the xenografts by direct injection. We observed high, immediate expression of MnSOD in the xenografts that persisted for 10 days following cessation of viral construct delivery. Delivery of the MnSOD construct resulted in a maximal 50% reduction in tumor growth compared with untreated controls. Our results suggest that MnSOD may be a tumor suppressor gene in the hamster cheek pouch model system.
Insights
Manganese superoxide dismutase (MnSOD) expression decreased during hamster cheek pouch carcinogenesis. Overexpressing MnSOD in tumors reduced growth by up to 50%, suggesting its role as a tumor suppressor.
Area of Science:
- Biochemistry
- Oncology
- Molecular Biology
Background:
- The antioxidant enzyme system protects cells from reactive oxygen species damage.
- Manganese superoxide dismutase (MnSOD) exhibits tumor suppressor gene-like activity.
- Understanding MnSOD's role in carcinogenesis is crucial for developing cancer therapies.
Purpose of the Study:
- To investigate MnSOD expression changes during hamster cheek pouch carcinogenesis.
- To evaluate the impact of MnSOD overexpression on tumor growth using an adenoviral vector.
Main Methods:
- Tumor induction in hamster cheek pouches using 7,12-dimethylbenz[alpha]anthracene.
- Immunohistochemistry and digital image analysis to assess MnSOD expression.
- Adenoviral vector-mediated MnSOD gene delivery to established xenografts in nude mice.
Main Results:
- A significant reduction in MnSOD expression was observed early in carcinogenesis and persisted throughout the study.
- Direct injection of an adenoviral vector resulted in high, sustained MnSOD expression in xenografts.
- MnSOD overexpression led to a maximum 50% reduction in tumor growth compared to controls.
Conclusions:
- MnSOD expression is downregulated during hamster cheek pouch carcinogenesis.
- MnSOD gene delivery effectively suppresses tumor growth in this model.
- These findings support MnSOD's function as a tumor suppressor gene in this experimental system.
