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dc.contributor.authorKAUSHIK, NEHA-
dc.date.accessioned2019-07-17T02:36:29Z-
dc.date.available2019-07-17T02:36:29Z-
dc.date.issued2019-02-
dc.identifier.citationCELL COMMUNICATION AND SIGNALING, v. 17, Page. 1-13en_US
dc.identifier.issn1478-811X-
dc.identifier.urihttps://biosignaling.biomedcentral.com/articles/10.1186/s12964-019-0322-x-
dc.identifier.urihttps://repository.hanyang.ac.kr/handle/20.500.11754/107505-
dc.description.abstractBackground: The existence of differentiated thyroid cells is critical to respond radioactive iodide treatment strategy in thyroid cancer, and loss of the differentiated phenotype is a trademark of iodide-refractive thyroid disease. While high-dose therapy has been beneficial to several cancer patients, many studies have indicated this clinical benefit was limited to patients having BRAF mutation. BRAF-targeted paired box gene-8 (PAX8), a thyroid-specific transcription factor, generally dysregulated in BRAF-mutated thyroid cancer. Methods: In this study, thyroid iodine-metabolizing gene levels were detected in BRAF-transformed thyroid cells after low and high dose of ionizing radiation. Also, an mRNA-targeted approach was used to figure out the underlying mechanism of low (0.01Gyx10 or 0.1Gy) and high (2Gy) radiation function on thyroid cancer cells after BRAF(V600E) mutation. Results: Low dose radiation (LDR)-induced PAX8 upregulation restores not only BRAF-suppressive sodium/iodide symporter (NIS) expression, one of the major protein necessary for iodine uptake in healthy thyroid, on plasma membrane but also regulate other thyroid metabolizing genes levels. Importantly, LDR-induced PAX8 results in decreased cellular transformation in BRAF-mutated thyroid cells. Conclusion: The present findings provide evidence that LDR-induced PAX8 acts as an important regulator for suppression of thyroid carcinogenesis through novel STAT3/miR-330-5p pathway in thyroid cancers.en_US
dc.description.sponsorshipThis work was supported by the Ministry of trade; industry & energy grant No. 20131610101840 and also by grant of the Korea Institute of Radiological and Medical Sciences (KIRAMS), funded by Ministry of Science and ICT (MIST), Republic of Korea (50535-2019).en_US
dc.language.isoenen_US
dc.publisherBMCen_US
dc.subjectLow dose radiationen_US
dc.subjectLDRen_US
dc.subjectThyroid canceren_US
dc.subjectPaired-box domain 8en_US
dc.subjectPAX8en_US
dc.subjectmiR-330-5pen_US
dc.subjectThyroglobulinen_US
dc.subjectTGen_US
dc.titleLow dose radiation regulates BRAF-induced thyroid cellular dysfunction and transformationen_US
dc.typeArticleen_US
dc.relation.no12-
dc.relation.volume17-
dc.identifier.doi10.1186/s12964-019-0322-x-
dc.relation.page1-13-
dc.relation.journalCELL COMMUNICATION AND SIGNALING-
dc.contributor.googleauthorKaushik, Neha-
dc.contributor.googleauthorKim, Min-Jung-
dc.contributor.googleauthorKaushik, Nagendra Kumar-
dc.contributor.googleauthorMyung, Jae Kyung-
dc.contributor.googleauthorChoi, Mi-Young-
dc.contributor.googleauthorKang, Jae-Hyeok-
dc.contributor.googleauthorCha, Hyuk-Jin-
dc.contributor.googleauthorKim, Cha-Soon-
dc.contributor.googleauthorNam, Seon-Young-
dc.contributor.googleauthorLee, Su-Jae-
dc.relation.code2019036141-
dc.sector.campusS-
dc.sector.daehakRESEARCH INSTITUTE[S]-
dc.sector.departmentTHE RESEARCH INSTITUTE FOR NATURAL SCIENCES-
dc.identifier.pidneha1987-


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