Interaction Between Cap- Derived Singlet Oxygen And Tumor Cell Protective Catalase: Update And Chances

Publication date: February 2018 Source:Clinical Plasma Medicine, Volume 9, Supplement Author(s): Georg Bauer Transformation of cells from various tissues requires NADPH oxidase-dependent generation of extracellular superoxide anions. These drive the proliferation, but also cause the elimination of malignant cells through the HOCl and the NO/peroxynitrite signaling pathways. These intercellular signaling pathways induce apoptosis selectively in malignant cells, due to site-specific concerted interaction of defined reactive oxygen and nitrogen species (ROS/RNS). Tumor progression requires the expression of membrane-associated catalase. This enzyme interferes with HOCl signaling through decomposition of H2O2, and with NO/peroxynitrite signaling through oxidation of NO and decomposition of peroxynitrite. Membrane-associated catalase has been found on all lines of bona fide tumor cells and represents a promising target for novel antitumor strategies. Inactivation of tumor cell-specific membrane-associated catalase reactivates intercellular ROS/RNS-dependent apoptosis-inducing signaling and leads to autocrine apoptotic selfdestruction of tumor cells. Model experiments with defined ROS and RNS led to the conclusion that CAP-derived singlet oxygen might lead to site-specific inactivation of catalase, followed by tumor cell-specific generation of secondary singlet oxygen and further inactivation of catalase. This then allows for subsequent reactivation of intercellular ROS/RNS-depe...
Source: Clinical Plasma Medicine - Category: Research Source Type: research