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      Biomarkers for enhancing the radiosensitivity of nasopharyngeal carcinoma

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          Abstract

          Nasopharyngeal carcinoma (NPC) is a common head and neck malignancy. The incidence of NPC is higher in Southern China and Southeast Asia compared with Western countries. Given its high radiosensitivity, the standard treatment for NPC is radiotherapy. However, radioresistance remains a serious obstacle to successful treatment. Radioresistance can cause local recurrence and distant metastases in some patients after treatment by radiation. Thus, special emphasis has been given to the discovery of effective radiosensitizers. This review aims to discuss the biomarkers, classified according to the main mechanisms of radiosensitization, which can enhance the sensitivity of NPC cells to ionizing radiation.

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          Protein kinase CK2: structure, regulation and role in cellular decisions of life and death.

          David W. Litchfield (2003)
          Protein kinase CK2 ('casein kinase II') has traditionally been classified as a messenger-independent protein serine/threonine kinase that is typically found in tetrameric complexes consisting of two catalytic (alpha and/or alpha') subunits and two regulatory beta subunits. Accumulated biochemical and genetic evidence indicates that CK2 has a vast array of candidate physiological targets and participates in a complex series of cellular functions, including the maintenance of cell viability. This review summarizes current knowledge of the structural and enzymic features of CK2, and discusses advances that challenge traditional views of this enzyme. For example, the recent demonstrations that individual CK2 subunits exist outside tetrameric complexes and that CK2 displays dual-specificity kinase activity raises new prospects for the precise elucidation of its regulation and cellular functions. This review also discusses a number of the mechanisms that contribute to the regulation of CK2 in cells, and will highlight emerging insights into the role of CK2 in cellular decisions of life and death. In this latter respect, recent evidence suggests that CK2 can exert an anti-apoptotic role by protecting regulatory proteins from caspase-mediated degradation. The mechanistic basis of the observation that CK2 is essential for viability may reside in part in this ability to protect cellular proteins from caspase action. Furthermore, this anti-apoptotic function of CK2 may contribute to its ability to participate in transformation and tumorigenesis.
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            Notch signaling: control of cell communication and cell fate.

            Eric Lai (2004)
            Notch is a transmembrane receptor that mediates local cell-cell communication and coordinates a signaling cascade present in all animal species studied to date. Notch signaling is used widely to determine cell fates and to regulate pattern formation; its dysfunction results in a tremendous variety of developmental defects and adult pathologies. This primer describes the mechanism of Notch signal transduction and how it is used to control the formation of biological patterns.
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              MDC1 is a mediator of the mammalian DNA damage checkpoint.

              Grant S Stewart, Bin Wang, Colin Bignell … (2003)
              To counteract the continuous exposure of cells to agents that damage DNA, cells have evolved complex regulatory networks called checkpoints to sense DNA damage and coordinate DNA replication, cell-cycle arrest and DNA repair. It has recently been shown that the histone H2A variant H2AX specifically controls the recruitment of DNA repair proteins to the sites of DNA damage. Here we identify a novel BRCA1 carboxy-terminal (BRCT) and forkhead-associated (FHA) domain-containing protein, MDC1 (mediator of DNA damage checkpoint protein 1), which works with H2AX to promote recruitment of repair proteins to the sites of DNA breaks and which, in addition, controls damage-induced cell-cycle arrest checkpoints. MDC1 forms foci that co-localize extensively with gamma-H2AX foci within minutes after exposure to ionizing radiation. H2AX is required for MDC1 foci formation, and MDC1 forms complexes with phosphorylated H2AX. Furthermore, this interaction is phosphorylation dependent as peptides containing the phosphorylated site on H2AX bind MDC1 in a phosphorylation-dependent manner. We have shown by using small interfering RNA (siRNA) that cells lacking MDC1 are sensitive to ionizing radiation, and that MDC1 controls the formation of damage-induced 53BP1, BRCA1 and MRN foci, in part by promoting efficient H2AX phosphorylation. In addition, cells lacking MDC1 also fail to activate the intra-S phase and G2/M phase cell-cycle checkpoints properly after exposure to ionizing radiation, which was associated with an inability to regulate Chk1 properly. These results highlight a crucial role for MDC1 in mediating transduction of the DNA damage signal.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Cancer Biol Med
                Journal ID (iso-abbrev): Cancer Biol Med
                Journal ID (publisher-id): CBM
                Title: Cancer Biology & Medicine
                Publisher: Chinese Anti-Cancer Association
                ISSN (Print): 2095-3941
                Publication date (Print and electronic): March 2015
                Publication date (Print): March 2015
                Volume: 12
                Issue: 1
                Pages: 23-32
                Affiliations
                [1]Department of Otorhinolaryngology, the First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China
                Author notes

                Correspondence to: Guo-Hua Hu

                E-mail: hghcq@ 123456sina.com

                Article
                Publisher ID: cbm-12-01-023
                DOI: 10.7497/j.issn.2095-3941.2014.0015
                PMC ID: 4383846
                PubMed ID: 25859408
                SO-VID: e4a2df8d-c3c7-48e6-a4cc-a4d6a91afabc
                Copyright © 2015 Cancer Biology & Medicine
                License:

                This work is licensed under a Creative Commons Attribution 3.0 Unported License. To view a copy of this license, visit http://creativecommons.org/licenses/by/3.0/

                History
                Date received : 12 October 2014
                Date accepted : 07 January 2015
                Categories
                Subject: Review

                Keywords: nasopharyngeal carcinoma (npc),radiotherapy,radiosensitization,biomarkers
                Data availability:
                Keywords: nasopharyngeal carcinoma (npc), radiotherapy, radiosensitization, biomarkers

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