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Inhibition of casein kinase 2 enhances the death ligand- and natural kiler cell-induced hepatocellular carcinoma cell death

DC FieldValueLanguage
dc.contributor.author김형란-
dc.contributor.author김건홍-
dc.contributor.author김세종-
dc.contributor.author김종선-
dc.date.accessioned2015-05-19T17:23:39Z-
dc.date.available2015-05-19T17:23:39Z-
dc.date.issued2008-
dc.identifier.issn0009-9104-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/108063-
dc.description.abstractRecent studies have shown that the inhibition of casein kinase 2 (CK2) sensitizes many cancer cells to Fas ligand- and tumour necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced apoptosis. However, it has not been demonstrated directly whether CK2 inhibition can also enhance the cytotoxicity of natural killer (NK) cells, which actually use the death ligands to kill cancer cells in vivo. To address whether NK cell-mediated cancer cell death is affected by the inhibition of CK2, we first checked whether the death ligand-induced apoptosis of hepatocellular carcinoma cells (HCCs) and HeLa were affected by CK2 inhibition. We then investigated the effect of CK2 inhibition on NK cytotoxicity against HCCs and HeLa cells and its mechanistic features. Inhibition of CK2 by emodin increased the apoptotic cell death of HepG2, Hep3B and HeLa when the cancer cell lines were treated with a soluble form of recombinant TRAIL or an agonistic antibody of Fas. This phenomenon appeared to be correlated with the expression level of death receptors on the cancer cell surface. More interestingly, the inhibition of CK2 also greatly increased the NK cell-mediated cancer cell killing. The NK cytotoxicity against the cancer cells increased about twofold when the target cells were pretreated with a specific CK2 inhibitor, emodin or 4,5,6,7-tetrabromobenzotriazole. Furthermore, the increase of the NK cytotoxicity against cancer cells by CK2 inhibition was granule-independent and mediated possibly by the death ligands on the NK cell surface. This suggests that CK2 inhibitors could be used to enhance the cytotoxicity of NK cells and consequently increase host tumour immunity.-
dc.description.statementOfResponsibilityopen-
dc.format.extent336~344-
dc.relation.isPartOfCLINICAL AND EXPERIMENTAL IMMUNOLOGY-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.subject.MESHApoptosis/drug effects-
dc.subject.MESHApoptosis/immunology-
dc.subject.MESHCarcinoma, Hepatocellular/immunology-
dc.subject.MESHCarcinoma, Hepatocellular/pathology*-
dc.subject.MESHCasein Kinase II/antagonists & inhibitors*-
dc.subject.MESHCasein Kinase II/physiology-
dc.subject.MESHCytoplasmic Granules/immunology-
dc.subject.MESHCytotoxicity, Immunologic/drug effects-
dc.subject.MESHCytotoxicity, Immunologic/immunology-
dc.subject.MESHEmodin/pharmacology-
dc.subject.MESHFas Ligand Protein/immunology-
dc.subject.MESHHumans-
dc.subject.MESHKiller Cells, Natural/immunology*-
dc.subject.MESHLiver Neoplasms/immunology-
dc.subject.MESHLiver Neoplasms/pathology*-
dc.subject.MESHProtein Kinase Inhibitors/pharmacology-
dc.subject.MESHRecombinant Proteins/immunology-
dc.subject.MESHTNF-Related Apoptosis-Inducing Ligand/immunology-
dc.subject.MESHTumor Cells, Cultured-
dc.titleInhibition of casein kinase 2 enhances the death ligand- and natural kiler cell-induced hepatocellular carcinoma cell death-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Microbiology (미생물학)-
dc.contributor.googleauthorH.-R. Kim-
dc.contributor.googleauthorK. Kim-
dc.contributor.googleauthorK.-H. Lee-
dc.contributor.googleauthorS. J. Kim-
dc.contributor.googleauthorJ. Kim-
dc.identifier.doi10.1111/j.1365-2249.2008.03622.x-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA01146-
dc.contributor.localIdA00289-
dc.contributor.localIdA00603-
dc.contributor.localIdA00921-
dc.relation.journalcodeJ00550-
dc.identifier.eissn1365-2249-
dc.identifier.pmid18336591-
dc.subject.keywordApoptosis/drug effects-
dc.subject.keywordApoptosis/immunology-
dc.subject.keywordCarcinoma, Hepatocellular/immunology-
dc.subject.keywordCarcinoma, Hepatocellular/pathology*-
dc.subject.keywordCasein Kinase II/antagonists & inhibitors*-
dc.subject.keywordCasein Kinase II/physiology-
dc.subject.keywordCytoplasmic Granules/immunology-
dc.subject.keywordCytotoxicity, Immunologic/drug effects-
dc.subject.keywordCytotoxicity, Immunologic/immunology-
dc.subject.keywordEmodin/pharmacology-
dc.subject.keywordFas Ligand Protein/immunology-
dc.subject.keywordHumans-
dc.subject.keywordKiller Cells, Natural/immunology*-
dc.subject.keywordLiver Neoplasms/immunology-
dc.subject.keywordLiver Neoplasms/pathology*-
dc.subject.keywordProtein Kinase Inhibitors/pharmacology-
dc.subject.keywordRecombinant Proteins/immunology-
dc.subject.keywordTNF-Related Apoptosis-Inducing Ligand/immunology-
dc.subject.keywordTumor Cells, Cultured-
dc.contributor.alternativeNameKim, Hyung Ran-
dc.contributor.alternativeNameKim, Kun Hong-
dc.contributor.alternativeNameKim, Se Jong-
dc.contributor.alternativeNameKim, Jong Sun-
dc.contributor.affiliatedAuthorKim, Hyung Ran-
dc.contributor.affiliatedAuthorKim, Kun Hong-
dc.contributor.affiliatedAuthorKim, Se Jong-
dc.contributor.affiliatedAuthorKim, Jong Sun-
dc.rights.accessRightsfree-
dc.citation.volume152-
dc.citation.number2-
dc.citation.startPage336-
dc.citation.endPage344-
dc.identifier.bibliographicCitationCLINICAL AND EXPERIMENTAL IMMUNOLOGY, Vol.152(2) : 336-344, 2008-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Microbiology (미생물학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Biochemistry and Molecular Biology (생화학-분자생물학교실) > 1. Journal Papers

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