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dc.contributor.authorKAUSHIKNEHA-
dc.date.accessioned2019-11-20T08:50:24Z-
dc.date.available2019-11-20T08:50:24Z-
dc.date.issued2017-02-
dc.identifier.citationSCIENTIFIC REPORTS, v. 7, Article no. 43361en_US
dc.identifier.issn2045-2322-
dc.identifier.urihttps://www.nature.com/articles/srep43361-
dc.identifier.urihttps://repository.hanyang.ac.kr/handle/20.500.11754/112656-
dc.description.abstractBreast cancer is a widely distributed type of cancer in women worldwide, and tumor relapse is the major cause of breast cancer death. In breast cancers, the acquisition of metastatic ability, which is responsible for tumor relapse and poor clinical outcomes, has been linked to the acquisition of the epithelial-mesenchymal transition (EMT) program and self-renewal traits (CSCs) via various signaling pathways. These phenomena confer resistance during current therapies, thus creating a major hurdle in radiotherapy/chemotherapy. The role of very low doses of radiation (LDR) in the context of EMT has not yet to be thoroughly explored. Here, we report that a 0.1 Gy radiation dose reduces cancer progression by deactivating the JAK1/STAT3 pathway. Furthermore, LDR exposure also reduces sphere formation and inhibits the self-renewal ability of breast cancer cells, resulting in an attenuated CD44(+)/CD24(-) population. Additionally, in vivo findings support our data, providing evidence that LDR is a promising option for future treatment strategies to prevent cancer metastasis in breast cancer cases.en_US
dc.description.sponsorshipThis work was supported by the Ministry of trade; industry & energy grant No. 20131610101840.en_US
dc.language.isoen_USen_US
dc.publisherNATURE PUBLISHING GROUPen_US
dc.subjectEPITHELIAL-MESENCHYMAL TRANSITIONen_US
dc.subjectTOTAL-BODY IRRADIATIONen_US
dc.subjectIONIZING-RADIATIONen_US
dc.subjectSTEM-CELLSen_US
dc.subjectX-RAYSen_US
dc.subjectGROWTHen_US
dc.subjectMETASTASISen_US
dc.subjectIMMUNEen_US
dc.subjectTRANSFORMATIONen_US
dc.subjectRESISTANCEen_US
dc.titleLow-dose radiation decreases tumor progression via the inhibition of the JAK1/STAT3 signaling axis in breast cancer cell linesen_US
dc.typeArticleen_US
dc.relation.volume7-
dc.identifier.doi10.1038/srep43361-
dc.relation.page1-9-
dc.relation.journalSCIENTIFIC REPORTS-
dc.contributor.googleauthorKaushik, Neha-
dc.contributor.googleauthorKim, Min-Jung-
dc.contributor.googleauthorKim, Rae-Kwon-
dc.contributor.googleauthorKaushik, Nagendra Kumar-
dc.contributor.googleauthorSeong, Ki Moon-
dc.contributor.googleauthorNam, Seon-Young-
dc.contributor.googleauthorLee, Su-Jae-
dc.relation.code2017003408-
dc.sector.campusS-
dc.sector.daehakRESEARCH INSTITUTE[S]-
dc.sector.departmentTHE RESEARCH INSTITUTE FOR NATURAL SCIENCES-
dc.identifier.pidneha1987-
dc.identifier.orcidhttp://orcid.org/0000-0002-4965-5046-
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RESEARCH INSTITUTE[S](부설연구소) > THE RESEARCH INSTITUTE FOR NATURAL SCIENCES(자연과학연구소) > Articles
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