Abstract 1409: C20orf52 regulates cell death by ionizing radiation via modulation of ROS generation in the mitochondria

Abstract

Abstract It is known that ROS exerts an important role in various intracellular physiological phenomena. Mitochondria and its molecules are one of major intracellular ROS source. Generation of ROS in normal cell condition is mainly caused by intracellular metabolic processes, but several extra-cellular stresses including ionizing radiation (IR) also increase ROS production. In this study, we tried to identify new molecular target that regulate ROS generation after IR irradiation, and confirmed the C20orf52 (also named as MTMG and Romo-1) as one of the new candidate. In recent report, C20orf52 was identified a regulator of ROS generation in the mitochondria, and it is located at integral mitochondrial inner-membrane. We constructed C20orf52 over-expressing HEK293 cell, and then showed that this C20orf52 over-expressing cells have a radio-resistance via suppression of ROS production by IR. Down-regulation of C20orf52 by siRNA treatment in several cancer cells increased cell death by IR. C20orf52 over-expression also increased mitochondrial potential and JNK phosphorylation in MAPKinase pathway induced by IR. Therefore we suggest that C20orf52 might modulate ROS production by IR and regulates cell death. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 1409.