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      mTOR-Mediated Antioxidant Activation in Solid Tumor Radioresistance

      review-article
      Author(s): 1 , 1 , 2 , 1 ,
      Publication date (Electronic):
      Journal: Journal of Oncology
      Publisher: Hindawi

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          Abstract

          Radiotherapy is widely used for the treatment of cancer patients, but tumor radioresistance presents serious therapy challenges. Tumor radioresistance is closely related to high levels of mTOR signaling in tumor tissues. Therefore, targeting the mTOR pathway might be a strategy to promote solid tumor sensitivity to ionizing radiation. Radioresistance is associated with enhanced antioxidant mechanisms in cancer cells. Therefore, examination of the relationship between mTOR signaling and antioxidant mechanism-linked radioresistance is required for effective radiotherapy. In particular, the effect of mTOR signaling on antioxidant glutathione induction by the Keap1-NRF2-xCT pathway is described in this review. This review is expected to assist in the identification of therapeutic adjuvants to increase the efficacy of radiotherapy.

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          Most cited references114

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          Ferroptosis, a new form of cell death: opportunities and challenges in cancer

          Yanhua Mou, Jun Jun Wang, Jinchun Wu … (2019)
          Ferroptosis is a novel type of cell death with distinct properties and recognizing functions involved in physical conditions or various diseases including cancers. The fast-growing studies of ferroptosis in cancer have boosted a perspective for its usage in cancer therapeutics. Here, we review the current findings of ferroptosis regulation and especially focus on the function of ncRNAs in mediating the process of cell ferroptotic death and on how ferroptosis was in relation to other regulated cell deaths. Aberrant ferroptosis in diverse cancer types and tissues were summarized, and we elaborated recent data about the novel actors of some “conventional” drugs or natural compounds as ferroptosis inducers in cancer. Finally, we deliberate future orientation for ferroptosis in cancer cells and current unsettled issues, which may forward the speed of clinical use of ferroptosis induction in cancer treatment.
          Article 0 comments Cited 795 times – based on 0 reviews     Review now
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            Superoxide dismutases: role in redox signaling, vascular function, and diseases.

            Tohru Fukai, Masuko Ushio-Fukai (2011)
            Excessive reactive oxygen species Revised abstract, especially superoxide anion (O₂•-), play important roles in the pathogenesis of many cardiovascular diseases, including hypertension and atherosclerosis. Superoxide dismutases (SODs) are the major antioxidant defense systems against (O₂•-), which consist of three isoforms of SOD in mammals: the cytoplasmic Cu/ZnSOD (SOD1), the mitochondrial MnSOD (SOD2), and the extracellular Cu/ZnSOD (SOD3), all of which require catalytic metal (Cu or Mn) for their activation. Recent evidence suggests that in each subcellular location, SODs catalyze the conversion of (O₂•-), H2O2, which may participate in cell signaling. In addition, SODs play a critical role in inhibiting oxidative inactivation of nitric oxide, thereby preventing peroxynitrite formation and endothelial and mitochondrial dysfunction. The importance of each SOD isoform is further illustrated by studies from the use of genetically altered mice and viral-mediated gene transfer. Given the essential role of SODs in cardiovascular disease, the concept of antioxidant therapies, that is, reinforcement of endogenous antioxidant defenses to more effectively protect against oxidative stress, is of substantial interest. However, the clinical evidence remains controversial. In this review, we will update the role of each SOD in vascular biologies, physiologies, and pathophysiologies such as atherosclerosis, hypertension, and angiogenesis. Because of the importance of metal cofactors in the activity of SODs, we will also discuss how each SOD obtains catalytic metal in the active sites. Finally, we will discuss the development of future SOD-dependent therapeutic strategies.
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              Antioxidants Maintain Cellular Redox Homeostasis by Elimination of Reactive Oxygen Species.

              Ting He, Shabnam Farrar, Linbao Ji … (2017)
              Reactive oxygen species (ROS) are produced by living cells as normal cellular metabolic byproduct. Under excessive stress conditions, cells will produce numerous ROS, and the living organisms eventually evolve series of response mechanisms to adapt to the ROS exposure as well as utilize it as the signaling molecules. ROS molecules would trigger oxidative stress in a feedback mechanism involving many biological processes, such as apoptosis, necrosis and autophagy. Growing evidences have suggested that ROS play a critical role as the signaling molecules throughout the entire cell death pathway. Overwhelming production of ROS can destroy organelles structure and bio-molecules, which lead to inflammatory response that is a known underpinning mechanism for the development of diabetes and cancer. Cytochrome P450 enzymes (CYP) are regarded as the markers of oxidative stress, can transform toxic metabolites into ROS, such as superoxide anion, hydrogen peroxide and hydroxyl radical which might cause injury of cells. Accordingly, cells have evolved a balanced system to neutralize the extra ROS, namely antioxidant systems that consist of enzymatic antioxidants such as superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidases (GPxs), thioredoxin (Trx) as well as the non-enzymatic antioxidants which collectively reduce oxidative state. Herein, we review the recent novel findings of cellular processes induced by ROS, and summarize the roles of cellular endogenous antioxidant systems as well as natural anti-oxidative compounds in several human diseases caused by ROS in order to illustrate the vital role of antioxidants in prevention against oxidative stress.
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                Author and article information

                Contributors
                Yu-Jin Jung:
                ORCID: https://orcid.org/0000-0002-4942-677X
                Journal
                Journal ID (nlm-ta): J Oncol
                Journal ID (iso-abbrev): J Oncol
                Journal ID (publisher-id): JO
                Title: Journal of Oncology
                Publisher: Hindawi
                ISSN (Print): 1687-8450
                ISSN (Electronic): 1687-8469
                Publication date Collection: 2019
                Publication date (Electronic): 20 December 2019
                Volume: 2019
                Electronic Location Identifier: 5956867
                Affiliations
                1Department of Biological Sciences and Institute of Life Science, Kangwon National University, Chuncheon 24341, Republic of Korea
                2Department of Chemistry, Kangwon National University, Chuncheon 24341, Republic of Korea
                Author notes

                Guest Editor: Vladimir Jurisic

                Author information
                https://orcid.org/0000-0003-4396-3723
                https://orcid.org/0000-0001-9892-8365
                https://orcid.org/0000-0003-4362-0990
                https://orcid.org/0000-0002-4942-677X
                Article
                DOI: 10.1155/2019/5956867
                PMC ID: 6942807
                PubMed ID: 31929797
                SO-VID: eb6c67ca-3435-4201-9496-1df1b5e2d1ed
                Copyright © Copyright © 2019 Yunseo Woo et al.
                License:

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 18 September 2019
                Date revision received : 20 November 2019
                Date accepted : 30 November 2019
                Funding
                Funded by: Ministry of Science, ICT and Future Planning
                Award ID: 2014M2B2A9030381
                Award ID: 2015M2B2A6028602
                Award ID: 2018R1D1A1B07049097
                Categories
                Subject: Review Article

                ScienceOpen disciplines: Oncology & Radiotherapy
                Data availability:
                ScienceOpen disciplines: Oncology & Radiotherapy

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