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CB-09. ARSENIC TRIOXIDE INDUCES BNIP3-DEPENDENT AUTOPHAGIC CELL DEATH IN MALIGNANT GLIOMA CELLS Takao Kanzawa, 1, 2 Isabelle Germano, 1 Hideaki Ito, 1, 2 Yasuko Kondo, 1, 2 and Seiji Kondo1, 2; 1Department of Neurosurgery, Mount Sinai School of Medicine, New York, NY; 2Department of Neurosurgery, University of Texas M.D. Anderson Cancer Center, Houston, TX; USA Arsenic trioxide As2O3 ; has shown considerable efficacy in treating hematological malignancies with induction of programmed cell death type I, apoptosis. However, the mechanisms underlying the antitumor effect of As2O3 on solid tumors are poorly defined. Previously, we reported that at clinically achievable concentrations 14 mM ; As2O3 induced autophagic cell death programmed cell death type II ; , but not apoptosis programmed cell death type I ; in human malignant glioma cell lines. Autophagy is a pivotal process for degradation and turnover of cytoplasmic organelles under certain stress conditions. To date, however, very little is known about the signal pathways leading to autophagic cell death in cancer therapy. In this study, using the green fluorescent protein GFP ; -tagged expression vector of microtubule-associated protein light chain 3 LC3 ; , a mammalian homologue of Apg8p Aut7p essential for autophagy in yeast, we first demonstrate that malignant glioma cells treated with As2O3 exhibited an increased punctate pattern of GFP-LC3, which is characteristic of autophagy. The expression levels of two forms of LC3 protein LC3-I and LC3-II ; were increased by the treatment with As2O3. We further demonstrate that As2O3 decreased mitochondrial membrane potential and activated the transcription of death-inducing mitochondrial protein, BNIP3, resulting in increasing the expression of BNIP3 in malignant glioma cells. Moreover, tumor cells transfected with BNIP3 gene presented autophagic expression pattern of GFP-LC3 without As2O3 treatment. These results suggest that As2O3-induced autophagy in malignant glioma cells is mediated by BNIP3. This study adds a new concept to characterize the pathways by which As2O3 acts to induce autophagic cell death in malignant gliomas and lexapro.

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