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dc.contributor.authorNa, J
dc.contributor.authorLee, C-H
dc.contributor.authorChung, J-K
dc.contributor.authorYoun, H
dc.date.accessioned2023-02-20T11:11:53Z
dc.date.issued2023-02-01
dc.identifier.issn1422-0067
dc.identifier.issn1422-0067
dc.identifier.otherARTN 2761
dc.identifier.urihttp://hdl.handle.net/10026.1/20441
dc.description.abstract

<jats:p>Improved therapeutic strategies are required to minimize side effects associated with radioiodine gene therapy to avoid unnecessary damage to normal cells and radiation-induced secondary malignancies. We previously reported that codon-optimized sodium iodide symporter (oNIS) enhances absorption of I-131 and that the brahma-associated gene 1 bromodomain (BRG1-BRD) causes inefficient DNA damage repair after high-energy X-ray therapy. To increase the therapeutic effect without applying excessive radiation, we considered the combination of oNIS and BRG1-BRD as gene therapy for the most effective radioiodine treatment. The antitumor effect of I-131 with oNIS or oNIS+BRD expression was examined by tumor xenograft models along with functional assays at the cellular level. The synergistic effect of both BRG1-BRD and oNIS gene overexpression resulted in more DNA double-strand breaks and led to reduced cell proliferation/survival rates after I-131 treatment, which was mediated by the p53/p21 pathway. We found increased p53, p21, and nucleophosmin 1 (NPM1) in oNIS- and BRD-expressing cells following I-131 treatment, even though the remaining levels of citrulline and protein arginine deiminase 4 (PAD4) were unchanged at the protein level.</jats:p>

dc.format.extent2761-2761
dc.format.mediumElectronic
dc.languageen
dc.language.isoeng
dc.publisherMDPI AG
dc.subjectsodium iodide symporter
dc.subjectradioiodine therapy
dc.subjectiodine-131
dc.subjectbrahma-related gene 1 bromodomain
dc.subjectradiosensitization
dc.subjectthyroid cancer
dc.titleOverexpression of Both Human Sodium Iodide Symporter (NIS) and BRG1-Bromodomain Synergistically Enhances Radioiodine Sensitivity by Stabilizing p53 through NPM1 Expression
dc.typejournal-article
dc.typeArticle
plymouth.author-urlhttps://www.ncbi.nlm.nih.gov/pubmed/36769088
plymouth.issue3
plymouth.volume24
plymouth.publisher-urlhttp://dx.doi.org/10.3390/ijms24032761
plymouth.publication-statusPublished online
plymouth.journalInternational Journal of Molecular Sciences
dc.identifier.doi10.3390/ijms24032761
plymouth.organisational-group/Plymouth
plymouth.organisational-group/Plymouth/Faculty of Health
plymouth.organisational-group/Plymouth/Faculty of Health/Peninsula Medical School
plymouth.organisational-group/Plymouth/REF 2021 Researchers by UoA
plymouth.organisational-group/Plymouth/REF 2021 Researchers by UoA/UoA01 Clinical Medicine
plymouth.organisational-group/Plymouth/Users by role
plymouth.organisational-group/Plymouth/Users by role/Academics
dc.publisher.placeSwitzerland
dcterms.dateAccepted2023-01-27
dc.rights.embargodate2023-2-21
dc.identifier.eissn1422-0067
dc.rights.embargoperiodNot known
rioxxterms.versionofrecord10.3390/ijms24032761
rioxxterms.licenseref.urihttp://www.rioxx.net/licenses/all-rights-reserved
rioxxterms.licenseref.startdate2023-02-01
rioxxterms.typeJournal Article/Review


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