title: Low-dose radiation decreases tumor progression via the inhibition of the JAK1/STAT3 signaling axis in breast cancer cell lines.
abstract: Breast 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.
authors.affiliation: Department of Life Science, Research Institute for Natural Sciences, Hanyang University, Seoul 04763, Republic of Korea.
authors.forename: Neha
authors.initials: N
authors.lastname: Kaushik
authors.affiliation: Laboratory of Radiation Exposure and Therapeutics, National Radiation Emergency Medical Center, Korea Institute of Radiological and Medical Sciences, Seoul, Korea.
authors.forename: Min-Jung
authors.initials: MJ
authors.lastname: Kim
authors.affiliation: The University of Texas MD Anderson Cancer Center, So Campus Research Bldg 1 (SCR2.2208), 1515 Holcombe Blvd. Unit 0903, Houston, TX 77030, USA.
authors.forename: Rae-Kwon
authors.initials: RK
authors.lastname: Kim
authors.affiliation: Plasma Bioscience Research Center, Department of Electrical and Biological Physics, Kwangwoon University, Seoul, 139-701, Republic of Korea.
authors.forename: Nagendra
authors.initials: N
authors.lastname: Kumar Kaushik
authors.affiliation: Laboratory of Radiation Exposure and Therapeutics, National Radiation Emergency Medical Center, Korea Institute of Radiological and Medical Sciences, Seoul, Korea.
authors.forename: Ki Moon
authors.initials: KM
authors.lastname: Seong
authors.affiliation: Radiation Health Institute, Korea Hydro and Nuclear Power Co. Ltd, Seoul, Korea.
authors.forename: Seon-Young
authors.initials: SY
authors.lastname: Nam
authors.affiliation: Department of Life Science, Research Institute for Natural Sciences, Hanyang University, Seoul 04763, Republic of Korea.
authors.forename: Su-Jae
authors.initials: SJ
authors.lastname: Lee
mesh_terms: D000818:Animals; D001943:Breast Neoplasms / Q000235:genetics / Q000378:metabolism / Q000473:pathology / Q000532:radiotherapy*; D045744:Cell Line, Tumor; D002465:Cell Movement; D004307:Dose-Response Relationship, Radiation; D058750:Epithelial-Mesenchymal Transition / Q000528:radiation effects*; D005260:Female; D005720:Gamma Rays / Q000627:therapeutic use*; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D018960:Hyaluronan Receptors / Q000235:genetics / Q000378:metabolism; D053613:Janus Kinase 1 / Q000037:antagonists & inhibitors / Q000235:genetics* / Q000378:metabolism; D061986:MCF-7 Cells; D051379:Mice; D008807:Mice, Inbred BALB C; D008819:Mice, Nude; D010957:Plasmids / Q000737:chemistry / Q000378:metabolism; D050796:STAT3 Transcription Factor / Q000037:antagonists & inhibitors / Q000235:genetics* / Q000378:metabolism; D015398:Signal Transduction / Q000235:genetics / Q000528:radiation effects*; D014162:Transfection; D047368:Tumor Burden / Q000528:radiation effects; D023041:Xenograft Model Antitumor Assays
chemical_list: C497483:CD44 protein, human; D018960:Hyaluronan Receptors; D050796:STAT3 Transcription Factor; C494086:STAT3 protein, human; C507904:JAK1 protein, human; D053613:Janus Kinase 1