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      Tumor cell survival pathways activated by photodynamic therapy: a molecular basis for pharmacological inhibition strategies

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          Abstract

          Photodynamic therapy (PDT) has emerged as a promising alternative to conventional cancer therapies such as surgery, chemotherapy, and radiotherapy. PDT comprises the administration of a photosensitizer, its accumulation in tumor tissue, and subsequent irradiation of the photosensitizer-loaded tumor, leading to the localized photoproduction of reactive oxygen species (ROS). The resulting oxidative damage ultimately culminates in tumor cell death, vascular shutdown, induction of an antitumor immune response, and the consequent destruction of the tumor. However, the ROS produced by PDT also triggers a stress response that, as part of a cell survival mechanism, helps cancer cells to cope with the PDT-induced oxidative stress and cell damage. These survival pathways are mediated by the transcription factors activator protein 1 (AP-1), nuclear factor E2-related factor 2 (NRF2), hypoxia-inducible factor 1 (HIF-1), nuclear factor κB (NF-κB), and those that mediate the proteotoxic stress response. The survival pathways are believed to render some types of cancer recalcitrant to PDT and alter the tumor microenvironment in favor of tumor survival. In this review, the molecular mechanisms are elucidated that occur post-PDT to mediate cancer cell survival, on the basis of which pharmacological interventions are proposed. Specifically, pharmaceutical inhibitors of the molecular regulators of each survival pathway are addressed. The ultimate aim is to facilitate the development of adjuvant intervention strategies to improve PDT efficacy in recalcitrant solid tumors.

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          Most cited references 392

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          HIFalpha targeted for VHL-mediated destruction by proline hydroxylation: implications for O2 sensing.

           M Ivan,  Theresa Kim,  A Salic (2001)
          HIF (hypoxia-inducible factor) is a transcription factor that plays a pivotal role in cellular adaptation to changes in oxygen availability. In the presence of oxygen, HIF is targeted for destruction by an E3 ubiquitin ligase containing the von Hippel-Lindau tumor suppressor protein (pVHL). We found that human pVHL binds to a short HIF-derived peptide when a conserved proline residue at the core of this peptide is hydroxylated. Because proline hydroxylation requires molecular oxygen and Fe(2+), this protein modification may play a key role in mammalian oxygen sensing.
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            NF-kappaB in cancer: from innocent bystander to major culprit.

            Nuclear factor of kappaB (NF-kappaB) is a sequence-specific transcription factor that is known to be involved in the inflammatory and innate immune responses. Although the importance of NF-KB in immunity is undisputed, recent evidence indicates that NF-kappaB and the signalling pathways that are involved in its activation are also important for tumour development. NF-kappaB should therefore receive as much attention from cancer researchers as it has already from immunologists.
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              AP-1: a double-edged sword in tumorigenesis.

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                Author and article information

                Contributors
                +31 (0)20 566 5573 , m.heger@amc.uva.nl
                Journal
                Cancer Metastasis Rev
                Cancer Metastasis Rev
                Cancer Metastasis Reviews
                Springer US (New York )
                0167-7659
                1573-7233
                29 October 2015
                29 October 2015
                2015
                : 34
                : 4
                : 643-690
                Affiliations
                [ ]Department of Experimental Surgery, Academic Medical Center, University of Amsterdam, Meibergdreef 9, 1105 AZ Amsterdam, The Netherlands
                [ ]Wellman Center for Photomedicine, Massachusetts General Hospital, Boston, MA USA
                [ ]Department of Dermatology, Harvard Medical School, Boston, MA USA
                [ ]Harvard-MIT Division of Health Sciences & Technology, Cambridge, MA USA
                Article
                9588
                10.1007/s10555-015-9588-7
                4661210
                26516076
                © The Author(s) 2015

                Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.

                Categories
                Non-Thematic Review
                Custom metadata
                © Springer Science+Business Media New York 2015

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