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      • Record: found
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      NOS1-, NOS3-, PIK3CA-, and MAPK-pathways in skin following radiation therapy

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          Abstract

          Background

          Essential molecular pathways such as the MAPK pathway, NO system, or the influence of PIK3CA as an oncogene are known to regulate fundamental signalling networks. However, few knowledge about their role in the occurrence of wound healing disorders (WHD) following radiation therapy (RT) exists. This study aims to evaluate the expression profiles of specific molecular pathway marker genes.

          Methods

          Expression profiles of the genes encoding MAPK, NOS1, NOS3, and PIK3CA were analyzed, by RT-PCR, in specimens from patients with and without a history of RT to the head and neck. Clinical data on the occurrence of cervical WHDs were analyzed.

          Results

          Expression analysis of patients with postoperative WHDs revealed a significant increase in MAPK expression compared to the control group without occurrence of postoperative WHDs. PIK3CA showed a significantly increased expression in patients with a history of RT. Expression analysis of all other investigated genes did not reveal significant differences.

          Conclusions

          This current study is able to show the influence of RT on different molecular pathways. This underlines the crucial role of specific molecular networks, responsible for the occurrence of long-term radiation toxicity such as WHDs. Additional studies should be carried out to identify possible starting points for therapeutic interventions.

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          Most cited references20

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          Nitric oxide: a cytotoxic activated macrophage effector molecule.

          John Hibbs, Read Taintor, Zdenek Vavrin … (1988)
          The experiments reported here identify nitric oxide as a molecular effector of activated macrophage induced cytotoxicity. Cytotoxic activated macrophages synthesize nitric oxide from a terminal guanidino nitrogen atom of L-arginine which is converted to L-citrulline without loss of the guanidino carbon atom. In addition, authentic nitric oxide gas causes the same pattern of cytotoxicity in L10 hepatoma cells as is induced by cytotoxic activated macrophages (iron loss as well as inhibition of DNA synthesis, mitochondrial respiration, and aconitase activity). The results suggest that nitric oxide is the precursor of nitrite/nitrate synthesized by cytotoxic activated macrophages and, via formation of iron-nitric oxide complexes and subsequent degradation of iron-sulfur prosthetic groups, an effector molecule.
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            Anti-Wrinkle and Anti-Inflammatory Effects of Active Garlic Components and the Inhibition of MMPs via NF-κB Signaling

            So-Ra Kim, Yu-Ri Jung, Hye Jin An … (2013)
            Skin aging is a multisystem degenerative process caused by several factors, such as, UV irradiation, stress, and smoke. Furthermore, wrinkle formation is a striking feature of photoaging and is associated with oxidative stress and inflammatory response. In the present study, we investigated whether caffeic acid, S-allyl cysteine, and uracil, which were isolated from garlic, modulate UVB-induced wrinkle formation and effect the expression of matrix-metalloproteinase (MMP) and NF-κB signaling. The results obtained showed that all three compounds significantly inhibited the degradation of type І procollagen and the expressions of MMPs in vivo and attenuated the histological collagen fiber disorder and oxidative stress in vivo. Furthermore, caffeic acid and S-allyl cysteine were found to decrease oxidative stress and inflammation by modulating the activities of NF-κB and AP-1, and uracil exhibited an indirect anti-oxidant effect by suppressing cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) expressions levels and downregulating transcriptional factors. These results suggest that the anti-wrinkle effects of caffeic acid, S-allyl cysteine, and uracil are due to anti-oxidant and/or anti-inflammatory effects. Summarizing, caffeic acid, S-allyl cysteine, and uracil inhibited UVB-induced wrinkle formation by modulating MMP via NF-κB signaling.
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              PIK3CA mutations in head and neck squamous cell carcinoma.

              G Su, Judy Ho, Spiros Manolidis … (2006)
              Recent studies have reported high frequencies of somatic mutations in the phosphoinositide-3-kinase catalytic alpha (PIK3CA) gene in several human solid tumors. Although gene amplifications of PIK3CA have been reported in head and neck squamous cell carcinoma (HNSCC), small mutation of the gene has not been evaluated in HNSCC previously. In this study, we examined the mutation frequency of PIK3CA in HNSCC. More than 75% of the somatic mutations of PIK3CA are clustered in the helical (exon 9) and kinase domains (exon 20). To investigate the possible role of PIK3CA in HNSCC tumorigenesis, exons 1, 4, 5, 6, 7, 9, and 20 of the gene were analyzed by direct genomic DNA sequencing in 38 HNSCC specimens. We identified four missense mutations in the seven exons of PIK3CA from 38 HNSCC specimens (11%). Three of the four mutations (i.e., H1047R, E542K, and E545K) have been previously reported as hotspot mutations. The remaining novel mutation, Y343C, is identified at exon 4 nucleotide 1028 A --> G. Three of the four mutations were shown to be somatic, whereas the fourth mutation (H1047R) was identified in a cell line. Interestingly, three of the four mutations identified were in pharyngeal cancer samples. These data provide evidence that oncogenic properties of PIK3CA contribute to the carcinogenesis of human head and neck cancers, especially in pharyngeal cancer. A specific kinase inhibitor to PIK3CA may potentially be an effective therapeutic reagent against HNSCC or pharyngeal cancer in particular.
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                Author and article information

                Contributors
                Steffen Koerdt: +49 89 4140 5616 , steffen.koerdt@tum.de
                Journal
                Journal ID (nlm-ta): Biomark Res
                Journal ID (iso-abbrev): Biomark Res
                Title: Biomarker Research
                Publisher: BioMed Central (London )
                ISSN (Electronic): 2050-7771
                Publication date (Electronic): 20 January 2017
                Publication date PMC-release: 20 January 2017
                Publication date Collection: 2017
                Volume: 5
                Electronic Location Identifier: 3
                Affiliations
                [1 ]ISNI 0000000123222966, GRID grid.6936.a, Department of Oral and Maxillofacial Surgery, , Technical University of Munich (TUM), ; Ismaninger Str. 22, D-81675 Munich, Germany
                [2 ]ISNI 0000 0001 0328 4908, GRID grid.5253.1, Department of Oral and Maxillofacial Surgery, , Heidelberg University Hospital, ; Im Neuenheimer Feld 400, D-69120 Heidelberg, Germany
                Article
                Publisher ID: 84
                DOI: 10.1186/s40364-017-0084-9
                PMC ID: 5251289
                SO-VID: ec856ade-66e8-4dd4-87f4-760475d9e201
                Copyright © © The Author(s). 2017
                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 : 19 October 2016
                Date accepted : 4 January 2017
                Categories
                Subject: Research
                Custom metadata
                issue-copyright-statement © The Author(s) 2017

                Keywords: radiation therapy,mapk,nos,pik3ca,pcr
                Data availability:
                Keywords: radiation therapy, mapk, nos, pik3ca, pcr

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