Full metadata record
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 이수재 | - |
dc.date.accessioned | 2018-02-13T02:40:17Z | - |
dc.date.available | 2018-02-13T02:40:17Z | - |
dc.date.issued | 2011-09 | - |
dc.identifier.citation | JOURNAL OF CELL SCIENCE, 2011, 124(18), P.3084-3094 | en_US |
dc.identifier.issn | 0021-9533 | - |
dc.identifier.uri | http://jcs.biologists.org/content/124/18/3084 | - |
dc.description.abstract | Brain tumors frequently recur or progress as focal masses after treatment with ionizing radiation. However, the mechanisms underlying the repopulation of tumor cells after radiation have remained unclear. In this study, we show that cellular signaling from Abelson murine leukemia viral oncogene homolog (Abl) to protein kinase Cd (PKC delta) is crucial for fractionated-radiation-induced expansion of glioma-initiating cell populations and acquisition of resistance to anticancer treatments. Treatment of human glioma cells with fractionated radiation increased Abl and PKC delta activity, expanded the CD133-positive (CD133(+)) cell population that possesses tumor-initiating potential and induced expression of glioma stem cell markers and self-renewal-related proteins. Moreover, cells treated with fractionated radiation were resistant to anticancer treatments. Small interfering RNA (siRNA)-mediated knockdown of PKC delta expression blocked fractionated-radiation-induced CD133(+) cell expansion and suppressed expression of glioma stem cell markers and self-renewal-related proteins. It also suppressed resistance of glioma cells to anticancer treatments. Similarly, knockdown of Abl led to a decrease in CD133(+) cell populations and restored chemotherapeutic sensitivity. It also attenuated fractionated-radiation-induced PKC delta activation, suggesting that Abl acts upstream of PKC delta. Collectively, these data indicate that fractionated radiation induces an increase in the glioma-initiating cell population, decreases cellular sensitivity to cancer treatment and implicates activation of Abl-PKC delta signaling in both events. These findings provide insights that might prove pivotal in the context of ionising-radiation-based therapeutic interventions for brain tumors. | en_US |
dc.description.sponsorship | This work was supported by the Korea Research Foundation (KRF) and Ministry of Education, Science and Technology (MEST), Korean government, through its National Nuclear Technology Program (2008-2003935) and Medical Research Center Program (2010-0091464). | en_US |
dc.language.iso | en | en_US |
dc.publisher | COMPANY OF BIOLOGISTS LTD | en_US |
dc.subject | Fractionated radiation | en_US |
dc.subject | PKC delta | en_US |
dc.subject | Abl | en_US |
dc.subject | Glioma stem-like cells | en_US |
dc.subject | Resistance to cancer treatments | en_US |
dc.subject | PROTEIN-KINASE-C | en_US |
dc.subject | HUMAN BRAIN-TUMORS | en_US |
dc.subject | STEM-CELLS | en_US |
dc.subject | MALIGNANT GLIOMAS | en_US |
dc.subject | GLIOBLASTOMA | en_US |
dc.subject | PROLIFERATION | en_US |
dc.subject | INHIBITION | en_US |
dc.subject | APOPTOSIS | en_US |
dc.subject | THERAPY | en_US |
dc.subject | DIFFERENTIATION | en_US |
dc.title | Importance of PKC delta signaling in fractionated-radiation-induced expansion of glioma-initiating cells and resistance to cancer treatment | en_US |
dc.type | Article | en_US |
dc.relation.no | 18 | - |
dc.relation.volume | 124 | - |
dc.identifier.doi | 10.1242/jcs.080119 | - |
dc.relation.page | 3084-3094 | - |
dc.relation.journal | JOURNAL OF CELL SCIENCE | - |
dc.contributor.googleauthor | Kim, Min-Jung | - |
dc.contributor.googleauthor | Kim, Rae-Kwon | - |
dc.contributor.googleauthor | Yoon, Chang-Hwan | - |
dc.contributor.googleauthor | Suh, Yong-Joon | - |
dc.contributor.googleauthor | Lee, Su-Jae | - |
dc.contributor.googleauthor | Kim, In-Gyu | - |
dc.contributor.googleauthor | An, Sung-Kwan | - |
dc.contributor.googleauthor | Hwang, Sang-Gu | - |
dc.contributor.googleauthor | Park, Myung-Jin | - |
dc.contributor.googleauthor | Chung, Hee-Young | - |
dc.relation.code | 2011204794 | - |
dc.sector.campus | S | - |
dc.sector.daehak | COLLEGE OF NATURAL SCIENCES[S] | - |
dc.sector.department | DEPARTMENT OF LIFE SCIENCE | - |
dc.identifier.pid | sj0420 | - |
dc.identifier.researcherID | 8066538700 | - |
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