Full metadata record
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 이수재 | - |
dc.date.accessioned | 2017-08-01T05:58:32Z | - |
dc.date.available | 2017-08-01T05:58:32Z | - |
dc.date.issued | 2015-10 | - |
dc.identifier.citation | ONCOGENE, v. 34, NO 42, Page. 5372-5382 | en_US |
dc.identifier.issn | 0950-9232 | - |
dc.identifier.issn | 1476-5594 | - |
dc.identifier.uri | http://www.nature.com/onc/journal/v34/n42/full/onc2014466a.html?foxtrotcallback=true | - |
dc.identifier.uri | http://hdl.handle.net/20.500.11754/28163 | - |
dc.description.abstract | Despite ionizing radiation (IR) is being widely used as a standard treatment for lung cancer, many evidences suggest that IR paradoxically promotes cancer malignancy. However, its molecular mechanisms underlying radiation-induced cancer progression remain obscure. Here, we report that exposure to fractionated radiation (2 Gy per day for 3 days) induces the secretion of granulocyte-colony-stimulating factor (G-CSF) that has been commonly used in cancer therapies to ameliorate neutropenia. Intriguingly, radiation-induced G-CSF promoted the migratory and invasive properties by triggering the epithelial-mesenchymal cell transition (EMT) in non-small-cell lung cancer cells (NSCLCs). By irradiation, G-CSF was upregulated transcriptionally by beta-catenin/TCF4 complex that binds to the promoter region of G-CSF as a transcription factor. Importantly, irradiation increased the stability of beta-catenin through the activation of PI3K/AKT (phosphatidylinositol 3-kinase/AKT), thereby upregulating the expression of G-CSF. Radiation-induced G-CSF is recognized by G-CSFR and transduced its intracellular signaling JAK/STAT3 (Janus kinase/ signal transducers and activators of transcription), thereby triggering EMT program in NSCLCs. Taken together, our findings suggest that the application of G-CSF in cancer therapies to ameliorate neutropenia should be reconsidered owing to its effect on cancer progression, and G-CSF could be a novel therapeutic target to mitigate the harmful effect of radiotherapy for the treatment of NSCLC. | en_US |
dc.description.sponsorship | This work was supported by the National Research Foundation (NRF) and Ministry of Science, ICT and Future Planning, Korean Government, through its National Nuclear Technology Program (2012M2A2A7035878), and the Ministry of Trade, Industry and Energy (Grant No: 20131610101840). | en_US |
dc.language.iso | en | en_US |
dc.publisher | NATURE PUBLISHING GROUP | en_US |
dc.subject | EPITHELIAL-MESENCHYMAL TRANSITION | en_US |
dc.subject | NF-KAPPA-B | en_US |
dc.subject | FACTOR G-CSF | en_US |
dc.subject | SIGNALING PATHWAY | en_US |
dc.subject | GM-CSF | en_US |
dc.subject | FEEDBACK LOOP | en_US |
dc.subject | BETA-CATENIN | en_US |
dc.subject | METASTASIS | en_US |
dc.subject | ACTIVATION | en_US |
dc.subject | CARCINOMA | en_US |
dc.title | Radiation promotes invasiveness of non-small-cell lung cancer cells through granulocyte-colony-stimulating factor | en_US |
dc.type | Article | en_US |
dc.relation.no | 42 | - |
dc.relation.volume | 34 | - |
dc.identifier.doi | 10.1038/onc.2014.466 | - |
dc.relation.page | 5372-5382 | - |
dc.relation.journal | ONCOGENE | - |
dc.contributor.googleauthor | Cui, Y-H | - |
dc.contributor.googleauthor | Suh, Y. | - |
dc.contributor.googleauthor | Lee, H-J | - |
dc.contributor.googleauthor | Yoo, K-C | - |
dc.contributor.googleauthor | Uddin, N. | - |
dc.contributor.googleauthor | Jeong, Y-J | - |
dc.contributor.googleauthor | Lee, J-S | - |
dc.contributor.googleauthor | Hwang, S-G | - |
dc.contributor.googleauthor | Nam, S-Y | - |
dc.contributor.googleauthor | Lee, S-J | - |
dc.relation.code | 2015000098 | - |
dc.sector.campus | S | - |
dc.sector.daehak | COLLEGE OF NATURAL SCIENCES[S] | - |
dc.sector.department | DEPARTMENT OF LIFE SCIENCE | - |
dc.identifier.pid | sj0420 | - |
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.