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      Dual roles of nitric oxide in the regulation of tumor cell response and resistance to photodynamic therapy

      a , * , a , b

      Redox Biology

      Elsevier

      ABC, ATP-binding cassette, ABCG2, ATP-binding cassette sub-family G member 2, AIF, apoptosis inducing factor, ALA, aminolevulinic acid, BCC, basal cell carcinoma, BCG, Bacillus Calmette-Guerin, CG, cholangiocarcinoma, CTL, cytotoxic T-lymphocyte, DR4/DR5, TRAIL death receptors, EGF, epithelial growth factor, EMT, epithelial mesenchymal transition, FASL, fas ligand, FDA, food and drug administration, 5-FU, 5-fluorouracil, GI, gastrointestinal, GSNO, S-nitrosoglutathione, HBD, hematoporphyrine-derivative, iNOS, inducible nitric oxide synthase, L-NAME, l-NG-Nitroarginine methyl ester, MAL, methylaminolevulinate, MDR, multidrug resistance, mPEG, monomethoxy-polyethylene glycol, NF-kB, nuclear factor kappa-light-chain-enhancer of activated B cells, NK, natural killer, 3O2, molecular singlet oxygen, 1O2, singlet oxygen, PARP, poly ADP ribose polymerase, Pba, pheophorbide a, PDT, photodynamic therapy, PS, photosensitizer, RIPT-1, receptor activity protein I, RKIP, Raf kinase inhibitor protein, ROS, reactive oxygen species, Ru (NO)(NO)(ONO)(pc), nitrosyl-phtalocyanin ruthenium complex, SCC, squamous cell carcinoma, SNAP, S-nitroso-N-acetylpenicillamine, SOD, superoxide dismutase, TNF-α, tumor necrosis factor alpha, TRAIL, TNF-related apoptosis-inducing ligand, TNF-R1/R2, tumor necrosis factor receptor 1/receptor 2, UV, ultraviolet, YY1, Yin Yang 1, Nitric oxide, Photodynamic therapy, Tumor response, Resistance, Molecular pathways.

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          Abstract

          Photodynamic therapy (PDT) against cancer has gained attention due to the successful outcome in some cancers, particularly those on the skin. However, there have been limitations to PDT applications in deep cancers and, occasionally, PDT treatment resulted in tumor recurrence. A better understanding of the underlying molecular mechanisms of PDT-induced cytotoxicity and cytoprotection should facilitate the development of better approaches to inhibit the cytoprotective effects and also augment PDT-mediated cytotoxicity. PDT treatment results in the induction of iNOS/NO in both the tumor and the microenvironment. The role of NO in cytotoxicity and cytoprotection was examined. The findings revealed that NO mediates its effects by interfering with a dysregulated pro-survival/anti-apoptotic NF-κB/Snail/YY1/RKIP loop which is often expressed in cancer cells. The cytoprotective effect of PDT-induced NO was the result of low levels of NO that activates the pro-survival/anti-apoptotic NF-κB, Snail, and YY1 and inhibits the anti-survival/pro-apoptotic and metastasis suppressor RKIP. In contrast, PDT-induced high levels of NO result in the inhibition of NF-kB, Snail, and YY1 and the induction of RKIP, all of which result in significant anti-tumor cytotoxicity. The direct role of PDT-induced NO effects was corroborated by the use of the NO inhibitor, l-NAME, which reversed the PDT-mediated cytotoxic and cytoprotective effects. In addition, the combination of the NO donor, DETANONOate, and PDT potentiated the PDT-mediated cytotoxic effects. These findings revealed a new mechanism of PDT-induced NO effects and suggested the potential therapeutic application of the combination of NO donors/iNOS inducers and PDT in the treatment of various cancers. In addition, the study suggested that the combination of PDT with subtoxic cytotoxic drugs will result in significant synergy since NO has been shown to be a significant chemo-immunosensitizing agent to apoptosis.

          Graphical abstract

          Highlights

          • PDT-mediated cytotoxic and cytoprotective effects depend also by the induction of NO from tumor.
          • The PDT-induced NO modulates the dysregulated NF-kB/Snail/RKIP loop.
          • The direct role of NO induction by PDT was corroborated by the use of the NO inhibitor, l-NAME.
          • The combination of an NO donor and PDT resulted in a increased cytotoxic effect, in vitro and in vivo.
          • Novel potential therapeutic applications are proposed for the use of PDT combined with NO donors.

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          Most cited references 87

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          Photodynamic therapy.

           Q Peng,  M Korbelik,  G Jori (1998)
          Photodynamic therapy involves administration of a tumor-localizing photosensitizing agent, which may require metabolic synthesis (i.e., a prodrug), followed by activation of the agent by light of a specific wavelength. This therapy results in a sequence of photochemical and photobiologic processes that cause irreversible photodamage to tumor tissues. Results from preclinical and clinical studies conducted worldwide over a 25-year period have established photodynamic therapy as a useful treatment approach for some cancers. Since 1993, regulatory approval for photodynamic therapy involving use of a partially purified, commercially available hematoporphyrin derivative compound (Photofrin) in patients with early and advanced stage cancer of the lung, digestive tract, and genitourinary tract has been obtained in Canada, The Netherlands, France, Germany, Japan, and the United States. We have attempted to conduct and present a comprehensive review of this rapidly expanding field. Mechanisms of subcellular and tumor localization of photosensitizing agents, as well as of molecular, cellular, and tumor responses associated with photodynamic therapy, are discussed. Technical issues regarding light dosimetry are also considered.
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            Necrotic death as a cell fate.

            Organismal homeostasis depends on an intricate balance between cell death and renewal. Early pathologists recognized that this balance could be disrupted by the extensive damage observed in internal organs during the course of certain diseases. This form of tissue damage was termed "necrosis", derived from the Greek "nekros" for corpse. As it became clear that the essential building block of tissue was the cell, necrosis came to be used to describe pathologic cell death. Until recently, necrotic cell death was believed to result from injuries that caused an irreversible bioenergetic compromise. The cell dying by necrosis has been viewed as a victim of extrinsic events beyond its control. However, recent evidence suggests that a cell can initiate its own demise by necrosis in a manner that initiates both inflammatory and/or reparative responses in the host. By initiating these adaptive responses, programmed cell necrosis may serve to maintain tissue and organismal integrity.
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              A multidrug resistance transporter from human MCF-7 breast cancer cells.

              MCF-7/AdrVp is a multidrug-resistant human breast cancer subline that displays an ATP-dependent reduction in the intracellular accumulation of anthracycline anticancer drugs in the absence of overexpression of known multidrug resistance transporters such as P glycoprotein or the multidrug resistance protein. RNA fingerprinting led to the identification of a 2.4-kb mRNA that is overexpressed in MCF-7/AdrVp cells relative to parental MCF-7 cells. The mRNA encodes a 655-aa [corrected] member of the ATP-binding cassette superfamily of transporters that we term breast cancer resistance protein (BCRP). Enforced expression of the full-length BCRP cDNA in MCF-7 breast cancer cells confers resistance to mitoxantrone, doxorubicin, and daunorubicin, reduces daunorubicin accumulation and retention, and causes an ATP-dependent enhancement of the efflux of rhodamine 123 in the cloned transfected cells. BCRP is a xenobiotic transporter that appears to play a major role in the multidrug resistance phenotype of MCF-7/AdrVp human breast cancer cells.
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                Author and article information

                Contributors
                Journal
                Redox Biol
                Redox Biol
                Redox Biology
                Elsevier
                2213-2317
                31 July 2015
                December 2015
                31 July 2015
                : 6
                : 311-317
                Affiliations
                [a ]Department of Medical and Biological Sciences, University of Udine, P.le Kolbe 4, 33100 Udine, Italy
                [b ]Department of Microbiology, Immunology and Molecular Genetics, University of California Los Angeles, Los Angeles, CA 90095, USA
                Author notes
                [* ]Corresponding author. Fax: +39 0432 494301. valentina.rapozzi@ 123456uniud.it
                Article
                S2213-2317(15)00087-7
                10.1016/j.redox.2015.07.015
                4556768
                26319434
                © 2015 The Authors

                This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).

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                Research Paper

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