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Forum on Immunopathological Diseases and Therapeutics
SJR: 0.309 SNIP: 0.041 CiteScore™: 0.18

ISSN Druckformat: 2151-8017
ISSN Online: 2151-8025

Archives: Volume 1, 2010 to Volume 7, 2016

Forum on Immunopathological Diseases and Therapeutics

DOI: 10.1615/ForumImmunDisTher.2011004418
pages 205-214

Pivotal Role of Nitric Oxide (NO) Induction by Photodynamic Therapy in Tumor Cells: Modification of the NF-κB/Snail/RKIP Survival/Anti-Apoptotic Loop

Valentina Rapozzi
Department of Medical Sciences University of Udine Udine, Italy
Benjamin Bonavida
Department of Microbiology, Immunology, & Molecular Genetics, David Geffen School of Medicine, Johnson Comprehensive Cancer Center, University of California at Los Angeles, Los Angeles, CA 90025-1747
Luigi E. Xodo
Department of Biomedical Sciences and Technologies, School of Medicine, University of Udine, Italy


Photodynamic therapy (PDT) is a therapeutic modality whose efficacy depends on several factors including the type of the photosensitizer, the light fluence, and cellular response. Cell recurrence and proliferation are problems that are unsolved in PDT; hence, new approaches are needed to increase the efficacy of PDT. Nitric oxide (NO), present in the tumor and in the tumoral microenvironment, has an important role as a modulator of PDT. Reports in the literature demonstrate that NO in tumors can exhibit pro- and anti-apoptotic properties by modulating different signalling pathways such as the NF-κB pathway and on downstream genes of the NF-κB/Snail/RKIP survival/anti-apoptotic circuitry. In this study, we present findings on the pivotal role played by NO in B78-H1 murine amelanocytic melanoma cells treated with pheophorbide a/PDT (Pba/PDT). The NO released by Pba/PDT modulated the NF-κB/Snail/RKIP loop leading to recurrence or death of the cells in a concentration-dependent manner. To sensitize cancer cells to photodynamic therapy, we demonstrate that the combined treatment of the photosensitizer Pheophorbide a with the NO donor, DETANONOate, resulted in tumor cell death.