Non-tumorigenic epithelial cells require anchorage to the extracellular matrix (ECM) in order to survive; however, it has been recognized that metastatic cancer cells must have the ability to survive in anchorage independence. Approximately 70% of epithelial ovarian cancer (EOC) cases are diagnosed after EOC cells have already metastasized, making EOC more difficult to treat. EOC cells shed from the primary tumor and accumulate in ascites in the peritoneal cavity before attaching and forming secondary tumors throughout the peritoneal cavity. A better understanding of the molecular mechanisms involved in the survival of this non-adhesive subset of cells that survive in anchorage independence in the ascites could lead to the development of improved chemotherapeutics and thus resulting in better survival rates of EOC patients. Striking increases of reactive oxygen species (ROS) mediated by ECM-detachment has been shown to inhibit survival in non-tumorigenic mammary epithelial cells. Furthermore, previous publications from our laboratory suggest that the antioxidant enzymes catalase, superoxide dismutase 1 (SOD1), and superoxide dismutase 2 (SOD2) are critical for metabolic maintenance and survival of ECM-detached breast cancer cells; however, many other antioxidant enzymes and their role in the survival of ECM-detached ovarian cancer cells have yet to be unveiled. Here, we have found that the antioxidant enzyme, Peroxiredoxin 2, is important in the survival of ECM-detached ovarian cancer cells, and elimination of this enzyme in SKOV3 cells results in decreased ability to survive in anchorage independence. Thus, our data reveal that Peroxiredoxin 2 may be an attractive target for the design of chemotherapeutics aimed at eliminating metastatic ovarian cancer cells. Given these data, we are working to understand the role of other members of the Peroxiredoxin family, namely Peroxiredoxin 1, in the survival of ovarian cancer cells in anchorage independence.

Citation Format: Calli A. Davison-Versagli. Peroxiredoxin 2 mediates the survival of ECM-detached ovarian cancer cells [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 5480. doi:10.1158/1538-7445.AM2017-5480