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Analysis of the Cellular Stress Response in MCF10A Cells Exposed to Combined Radio Frequency Radiation

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dc.contributor.authorKim, Han-Na-
dc.contributor.authorHan, Na-Kyung-
dc.contributor.authorHong, Mi-Na-
dc.contributor.authorChi, Sung-Gil-
dc.contributor.authorLee, Yun-Sil-
dc.contributor.authorKim, Taehong-
dc.contributor.authorPack, Jeong-Ki-
dc.contributor.authorChoi, Hyung-Do-
dc.contributor.authorKim, Nam-
dc.contributor.authorLee, Jae-Seon-
dc.date.accessioned2021-09-06T08:35:32Z-
dc.date.available2021-09-06T08:35:32Z-
dc.date.created2021-06-19-
dc.date.issued2012-03-
dc.identifier.issn0449-3060-
dc.identifier.urihttps://scholar.korea.ac.kr/handle/2021.sw.korea/105431-
dc.description.abstractExposure to environmental stressors can be measured by monitoring the cellular stress response in target cells. Here, we used the cellular stress response to investigate whether single or combined radio frequency (RF) radiation could induce stress response in human cells. Cellular stress responses in MCF10A human breast epithelial cells were characterized after exposure to 4 h of RF radiation [code division multiple access (CDMA) or CDMA plus wideband CDMA (WCDMA)] or 2 h RF radiation on 3 consecutive days. Specific absorption rate (SAR) was 4.0 W/kg for CDMA signal alone exposure and 2.0 W/kg each, 4.0 W/kg in total for combined CDMA plus WCDMA signals. Expression levels and phosphorylation states of specific heat shock proteins (HSPs) and mitogen-activated protein kinases (MAPKs) were analyzed by Western blot. It was found that HSP27 and ERK1/2 phosphorylations are the most sensitive markers of the stress response in MCF10A cells exposed to heat shock or ionizing radiation. Using these markers, we demonstrated that neither one-time nor repeated single (CDMA alone) or combined (CDMA plus WCDMA) RF radiation exposure significantly altered HSP27 and ERK1/2 phosphorylations in MCF10A cells (p > 0.05). The lack of a statistically significant alteration in HSP27 and ERK1/2 phosphorylations suggests that single or combined RF radiation exposure did not elicit activation of HSP27 and ERK1/2 in MCF10A cells.-
dc.languageEnglish-
dc.language.isoen-
dc.publisherOXFORD UNIV PRESS-
dc.subjectHEAT-SHOCK PROTEINS-
dc.subjectELECTROMAGNETIC-FIELDS-
dc.subjectRADIOFREQUENCY RADIATION-
dc.subjectGENE-EXPRESSION-
dc.subjectMICROWAVE IRRADIATION-
dc.subject1.8 GHZ-
dc.subjectKINASE-
dc.subjectPHOSPHORYLATION-
dc.subjectHSP70-
dc.subjectINDUCTION-
dc.titleAnalysis of the Cellular Stress Response in MCF10A Cells Exposed to Combined Radio Frequency Radiation-
dc.typeArticle-
dc.contributor.affiliatedAuthorChi, Sung-Gil-
dc.identifier.doi10.1269/jrr.11048-
dc.identifier.scopusid2-s2.0-84863442265-
dc.identifier.wosid000307196400003-
dc.identifier.bibliographicCitationJOURNAL OF RADIATION RESEARCH, v.53, no.2, pp.176 - 183-
dc.relation.isPartOfJOURNAL OF RADIATION RESEARCH-
dc.citation.titleJOURNAL OF RADIATION RESEARCH-
dc.citation.volume53-
dc.citation.number2-
dc.citation.startPage176-
dc.citation.endPage183-
dc.type.rimsART-
dc.type.docTypeArticle-
dc.description.journalClass1-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.relation.journalResearchAreaLife Sciences & Biomedicine - Other Topics-
dc.relation.journalResearchAreaOncology-
dc.relation.journalResearchAreaRadiology, Nuclear Medicine & Medical Imaging-
dc.relation.journalWebOfScienceCategoryBiology-
dc.relation.journalWebOfScienceCategoryOncology-
dc.relation.journalWebOfScienceCategoryRadiology, Nuclear Medicine & Medical Imaging-
dc.subject.keywordPlusHEAT-SHOCK PROTEINS-
dc.subject.keywordPlusELECTROMAGNETIC-FIELDS-
dc.subject.keywordPlusRADIOFREQUENCY RADIATION-
dc.subject.keywordPlusGENE-EXPRESSION-
dc.subject.keywordPlusMICROWAVE IRRADIATION-
dc.subject.keywordPlus1.8 GHZ-
dc.subject.keywordPlusKINASE-
dc.subject.keywordPlusPHOSPHORYLATION-
dc.subject.keywordPlusHSP70-
dc.subject.keywordPlusINDUCTION-
dc.subject.keywordAuthorRF radiation-
dc.subject.keywordAuthorHSP27-
dc.subject.keywordAuthorERK1/2-
dc.subject.keywordAuthorMCF10A cells-
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