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      Role of metabolism in cancer cell radioresistance and radiosensitization methods

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          Abstract

          Background

          Radioresistance is a major factor leading to the failure of radiotherapy and poor prognosis in tumor patients. Following the application of radiotherapy, the activity of various metabolic pathways considerably changes, which may result in the development of resistance to radiation.

          Main body

          Here, we discussed the relationships between radioresistance and mitochondrial and glucose metabolic pathways, aiming to elucidate the interplay between the tumor cell metabolism and radiotherapy resistance. In this review, we additionally summarized the potential therapeutic targets in the metabolic pathways.

          Short conclusion

          The aim of this review was to provide a theoretical basis and relevant references, which may lead to the improvement of the sensitivity of radiotherapy and prolong the survival of cancer patients.

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          Most cited references147

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          Lactate: a metabolic key player in cancer.

          Franziska Hirschhaeuser, Ulrike Sattler, Wolfgang Mueller-Klieser (2011)
          Increased glucose uptake and accumulation of lactate, even under normoxic conditions (i.e., aerobic glycolysis or the Warburg Effect), is a common feature of cancer cells. This phenomenon clearly indicates that lactate is not a surrogate of tumor hypoxia. Tumor lactate can predict for metastases and overall survival of patients, as shown by several studies of different entities. Metastasis of tumors is promoted by lactate-induced secretion of hyaluronan by tumor-associated fibroblasts that create a milieu favorable for migration. Lactate itself has been found to induce the migration of cells and cell clusters. Furthermore, radioresistance has been positively correlated with lactate concentrations, suggesting an antioxidative capacity of lactate. Findings on interactions of tumor metabolites with immune cells indicate a contribution of lactate to the immune escape. Furthermore, lactate bridges the gap between high lactate levels in wound healing, chronic inflammation, and cancer development. Tumor cells ensure sufficient oxygen and nutrient supply for proliferation through lactate-induced secretion of VEGF, resulting in the formation of new vessels. In summary, accumulation of lactate in solid tumors is a pivotal and early event in the development of malignancies. The determination of lactate should enter further clinical trials to confirm its relevance in cancer biology. ©2011 AACR
          Article 0 comments Cited 414 times – based on 0 reviews     Review now
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            Hypoxia-inducible factors, stem cells, and cancer.

            Brian Keith, M. Celeste Simon (2007)
            Regions of severe oxygen deprivation (hypoxia) arise in tumors due to rapid cell division and aberrant blood vessel formation. The hypoxia-inducible factors (HIFs) mediate transcriptional responses to localized hypoxia in normal tissues and in cancers and can promote tumor progression by altering cellular metabolism and stimulating angiogenesis. Recently, HIFs have been shown to activate specific signaling pathways such as Notch and the expression of transcription factors such as Oct4 that control stem cell self renewal and multipotency. As many cancers are thought to develop from a small number of transformed, self-renewing, and multipotent "cancer stem cells," these results suggest new roles for HIFs in tumor progression.
            Article 0 comments Cited 374 times – based on 0 reviews     Review now
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              FBW7 ubiquitin ligase: a tumour suppressor at the crossroads of cell division, growth and differentiation.

              Markus Welcker, Bruce Clurman (2008)
              FBW7 (F-box and WD repeat domain-containing 7) is the substrate recognition component of an evolutionary conserved SCF (complex of SKP1, CUL1 and F-box protein)-type ubiquitin ligase. SCF(FBW7) degrades several proto-oncogenes that function in cellular growth and division pathways, including MYC, cyclin E, Notch and JUN. FBW7 is also a tumour suppressor, the regulatory network of which is perturbed in many human malignancies. Numerous cancer-associated mutations in FBW7 and its substrates have been identified, and loss of FBW7 function causes chromosomal instability and tumorigenesis. This Review focuses on structural and functional aspects of FBW7 and its role in the development of cancer.
              Article 0 comments Cited 369 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Wei Xiong: 86-731-8480-5412 , xiongwei@csu.edu.cn
                Zhaoyang Zeng: zengzhaoyang@csu.edu.cn
                Journal
                Journal ID (nlm-ta): J Exp Clin Cancer Res
                Journal ID (iso-abbrev): J. Exp. Clin. Cancer Res
                Title: Journal of Experimental & Clinical Cancer Research : CR
                Publisher: BioMed Central (London )
                ISSN (Print): 0392-9078
                ISSN (Electronic): 1756-9966
                Publication date (Electronic): 23 April 2018
                Publication date PMC-release: 23 April 2018
                Publication date Collection: 2018
                Volume: 37
                Electronic Location Identifier: 87
                Affiliations
                [1 ]ISNI 0000 0004 1757 7615, GRID grid.452223.0, The Key Laboratory of Carcinogenesis of the Chinese Ministry of Health, , Xiangya Hospital, Central South University, ; Changsha, Hunan China
                [2 ]ISNI 0000 0001 0379 7164, GRID grid.216417.7, The Key Laboratory of Carcinogenesis and Cancer Invasion of the Chinese Ministry of Education, , Cancer Research Institute, Central South University, ; Changsha, Hunan China
                [3 ]GRID grid.431010.7, Hunan Key Laboratory of Nonresolving Inflammation and Cancer, Disease Genome Research Center, , The Third Xiangya Hospital, Central South University, ; Changsha, Hunan China
                [4 ]ISNI 0000 0001 0379 7164, GRID grid.216417.7, Hunan Key Laboratory of Translational Radiation Oncology, , Hunan Cancer Hospital and the Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, ; Changsha, Hunan China
                [5 ]ISNI 0000 0001 0675 4725, GRID grid.239578.2, Department of Cancer Biology, , Lerner Research Institute, Cleveland Clinic, ; Cleveland, Ohio USA
                Article
                Publisher ID: 758
                DOI: 10.1186/s13046-018-0758-7
                PMC ID: 5914062
                PubMed ID: 29688867
                SO-VID: 2900e517-4c2c-45aa-9099-cdd483d2b456
                Copyright © © The Author(s). 2018
                License:

                Open AccessThis 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. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

                History
                Date received : 18 December 2017
                Date accepted : 10 April 2018
                Funding
                Funded by: FundRef http://dx.doi.org/10.13039/501100001809, National Natural Science Foundation of China;
                Award ID: 81472531
                Award ID: 81472595
                Award ID: 81672688
                Award Recipient :
                Categories
                Subject: Review
                Custom metadata
                issue-copyright-statement © The Author(s) 2018

                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: radiotherapy,radioresistance,metabolic pathway,sensitivity,cancer
                Data availability:
                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: radiotherapy, radioresistance, metabolic pathway, sensitivity, cancer

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