Because
reactive oxygen species (ROS) are naturally produced as a consequence of aerobic metabolism, cells have developed a sophisticated set of
antioxidant molecules to prevent the toxic accumulation of these species. However, compared with normal cells, malignant cells often exhibit increased levels of intracellular ROS and altered levels of
antioxidant molecules. The resulting endogenous oxidative stress favors
tumor growth by promoting genetic instability, cell proliferation and angiogenesis. In this context, we assessed the influence of
catalase overexpression on the sensitivity of
breast cancer cells towards various anticancer treatments. Our data show that
catalase overexpression in MCF-7 cells leads to a 7-fold increase in
catalase activity but provokes a 40% decrease in the expression of both
glutathione peroxidase and
peroxiredoxin II. Interestingly, proliferation and migration capacities of MCF-7 cells were impaired by the overexpression of
catalase, as compared to parental cells. Regarding their sensitivity to anticancer treatments, we observed that cells overexpressing
catalase were more sensitive to
paclitaxel,
etoposide and
arsenic trioxide. However, no effect was observed on the cytotoxic response to ionizing radiations,
5-fluorouracil,
cisplatin or
doxorubicin. Finally, we observed that
catalase overexpression protects
cancer cells against the
pro-oxidant combination of ascorbate and
menadione, suggesting that changes in the expression of
antioxidant enzymes could be a mechanism of resistance of
cancer cells towards redox-based chemotherapeutic drugs.