211 237

Cited 23 times in

Protein kinase casein kinase 2-mediated upregulation of N-cadherin confers anoikis resistance on esophageal carcinoma cells.

DC FieldValueLanguage
dc.contributor.author김성호-
dc.contributor.author육종인-
dc.contributor.author고현석-
dc.contributor.author김건홍-
dc.contributor.author김성락-
dc.date.accessioned2014-12-19T17:28:17Z-
dc.date.available2014-12-19T17:28:17Z-
dc.date.issued2012-
dc.identifier.issn1541-7786-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/91469-
dc.description.abstractPreviously, we reported that high PKCK2 activity could protect cancer cells from death receptor-mediated apoptosis through phosphorylation of procaspase-2. Because anoikis is another form of apoptosis, we asked whether PKCK2 could similarly confer resistance to anoikis on cancer cells. Human esophageal squamous cancer cell lines with high PKCK2 activity (HCE4 and HCE7) were anoikis-resistant, whereas cell lines with low PKCK2 activity (TE2 and TE3) were anoikis-sensitive. Because the cells showed different sensitivity to anoikis, we compared the expression of cell adhesion molecules between anoikis-sensitive TE2 and anoikis-resistant HCE4 cells using cDNA microarray. We found that E-cadherin is expressed only in TE2 cells; whereas N-cadherin is expressed instead of E-cadherin in HCE4 cells. To examine whether PKCK2 activity could determine the type of cadherin expressed, we first increased intracellular PKCK2 activity in TE2 cells by overexpressing the PKCK2α catalytic subunit using lentivirus and found that high PKCK2 activity could switch cadherin expression from type E to N and confer anoikis resistance. Conversely, a decrease in PKCK2 activity in HCE4 cells by knockdown of PKCK2α catalytic subunit using shRNA induced N- to E-cadherin switching and the anoikis-resistant cells became sensitive. In addition, N-cadherin expression correlated with PKB/Akt activation and increased invasiveness. We conclude that high intracellular PKCK2 activity confers anoikis resistance on esophageal cancer cells by inducing E- to N-cadherin switching.-
dc.description.statementOfResponsibilityopen-
dc.relation.isPartOfMOLECULAR CANCER RESEARCH-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.titleProtein kinase casein kinase 2-mediated upregulation of N-cadherin confers anoikis resistance on esophageal carcinoma cells.-
dc.typeArticle-
dc.contributor.collegeCollege of Dentistry (치과대학)-
dc.contributor.departmentDept. of Oral Pathology (구강병리학)-
dc.contributor.googleauthorHyeonseok Ko-
dc.contributor.googleauthorSeongrak Kim-
dc.contributor.googleauthorCheng-Hao Jin-
dc.contributor.googleauthorEunjung Lee-
dc.contributor.googleauthorSunyoung Ham-
dc.contributor.googleauthorJong In Yook-
dc.contributor.googleauthorKunhong Kim-
dc.identifier.doi10.1158/1541-7786.MCR-12-0261-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA00590-
dc.contributor.localIdA02536-
dc.contributor.localIdA00150-
dc.contributor.localIdA00289-
dc.contributor.localIdA00565-
dc.relation.journalcodeJ02253-
dc.identifier.eissn1557-3125-
dc.contributor.alternativeNameJin, Cheng Hao-
dc.contributor.alternativeNameYook, Jong In-
dc.contributor.alternativeNameKo, Hyeon Seok-
dc.contributor.alternativeNameKim, Kun Hong-
dc.contributor.alternativeNameKim, Seong Rak-
dc.contributor.affiliatedAuthorJin, Cheng Hao-
dc.contributor.affiliatedAuthorYook, Jong In-
dc.contributor.affiliatedAuthorKo, Hyeon Seok-
dc.contributor.affiliatedAuthorKim, Kun Hong-
dc.contributor.affiliatedAuthorKim, Seong Rak-
dc.citation.volume10-
dc.citation.number8-
dc.citation.startPage1032-
dc.citation.endPage1038-
dc.identifier.bibliographicCitationMOLECULAR CANCER RESEARCH, Vol.10(8) : 1032-1038, 2012-
Appears in Collections:
2. College of Dentistry (치과대학) > Dept. of Oral Pathology (구강병리학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Biochemistry and Molecular Biology (생화학-분자생물학교실) > 1. Journal Papers

qrcode

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.