Attenuation of catalase activity in the malignant phenotype plays a functional role in an in vitro model for tumor progression

Ashok Gupta, Brent Butts, Kevin A. Kwei, Katerina Dvorakova, Steven P. Stratton, Margaret M. Briehl, G. Tim Bowden

Research output: Contribution to journalArticle

65 Scopus citations

Abstract

We have developed an in vitro model to study the molecular mechanisms of tumor progression. Using repeated treatments with ionizing radiation or N-methyl-N′-nitro-N-nitrosoguanidine (MNNG), we caused malignant progression of a papilloma producing mouse keratinocyte cell line, 308 cells. In a previous study we have shown that the malignant variants of 308 cells have elevated reactive oxygen species (ROS) levels, and have established a functional role for the pro-oxidant state in the progressed phenotype (Carcinogenesis 20 (1999) 2063). In this study, we have evaluated the status of intracellular defense mechanisms for ROS scavenging in the progressed phenotype to identify sources that contribute to their pro-oxidant state. Our results demonstrate that a reduction in several anti-oxidant defense mechanisms, including catalase and glutathione S-transferase mu, correlates with the emergence of the malignant phenotype. We provide evidence that attenuation of catalase activity may play a functional role in the malignant progression of mouse keratinocytes.

Original languageEnglish (US)
Pages (from-to)115-125
Number of pages11
JournalCancer Letters
Volume173
Issue number2
DOIs
StatePublished - Nov 28 2001

Keywords

  • Catalase
  • Reactive oxygen species
  • Skin cancer
  • Tumor progression

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

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