Cited 6 times in
Adherens junction-dependent PI3K/Akt activation induces resistance to genotoxin-induced cell death in differentiated intestinal epithelial cells.
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 김원호 | - |
dc.contributor.author | 김태일 | - |
dc.contributor.author | 양경민 | - |
dc.contributor.author | 채보아 | - |
dc.date.accessioned | 2015-04-24T16:20:33Z | - |
dc.date.available | 2015-04-24T16:20:33Z | - |
dc.date.issued | 2009 | - |
dc.identifier.issn | 0006-291X | - |
dc.identifier.uri | https://ir.ymlib.yonsei.ac.kr/handle/22282913/103351 | - |
dc.description.abstract | The crypt-villi axis of intestinal mucosa maintains homeostasis by renewal of epithelia, and also exhibits different properties from undifferentiated to terminally differentiated cells. We investigated differential susceptibility to genotoxin-induced cell death, based on the degree of differentiation of epithelial cells, and its mechanism. Differentiation was induced by post-confluence culture in Caco-2 cells. Methyl methanesulfonate (MMS), a direct-acting DNA alkylating agent, was used for genotoxin-induced cell death. Compared to subconfluent Caco-2 cells, 7 days post-confluent cells showed resistance to MMS-induced cell death. With increasing expression of adherens junction components of E-cadherin and beta-catenin, E-cadherin and p-Akt expression increased in 7 days post-confluent Caco-2 cells, and in human intestinal tissue, expression of E-cadherin and p-Akt also increased in the upper portion of villi, compared to the crypt. Inhibition of cell-cell adhesion using EGTA decreased Akt phosphorylation, which was reversed by calcium restoration. Akt phosphorylation by calcium-mediated cell-cell adhesion was more prominent in differentiated cells. In addition, treatment of a PI3K inhibitor, LY294002, inhibited Akt phosphorylation by calcium-mediated cell-cell adhesion. Finally, the differential sensitivity to MMS-induced cell death between subconfluent and 7 days post-confluent Caco-2 cells was eliminated by inhibiting cell-cell adhesion or PI3K. Our data demonstrated that cell adhesion-mediated PI3K/Akt activation could be one of the important mechanisms of resistance to genotoxin-induced cell death in differentiated epithelial cells. | - |
dc.description.statementOfResponsibility | open | - |
dc.format.extent | 738~743 | - |
dc.relation.isPartOf | BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | - |
dc.rights | CC BY-NC-ND 2.0 KR | - |
dc.rights.uri | https://creativecommons.org/licenses/by-nc-nd/2.0/kr/ | - |
dc.subject.MESH | Adherens Junctions/enzymology* | - |
dc.subject.MESH | Apoptosis* | - |
dc.subject.MESH | Caco-2 Cells | - |
dc.subject.MESH | Cadherins/metabolism | - |
dc.subject.MESH | Calcium/metabolism | - |
dc.subject.MESH | Cell Adhesion/drug effects | - |
dc.subject.MESH | Cell Differentiation | - |
dc.subject.MESH | Chromones/pharmacology | - |
dc.subject.MESH | Cyclin-Dependent Kinase Inhibitor p21/biosynthesis | - |
dc.subject.MESH | Drug Resistance* | - |
dc.subject.MESH | Humans | - |
dc.subject.MESH | Intestinal Mucosa/cytology | - |
dc.subject.MESH | Intestinal Mucosa/drug effects* | - |
dc.subject.MESH | Intestinal Mucosa/enzymology | - |
dc.subject.MESH | Methyl Methanesulfonate/pharmacology | - |
dc.subject.MESH | Morpholines/pharmacology | - |
dc.subject.MESH | Mutagens/pharmacology* | - |
dc.subject.MESH | NF-kappa B/metabolism | - |
dc.subject.MESH | Phosphatidylinositol 3-Kinases/antagonists & inhibitors | - |
dc.subject.MESH | Phosphatidylinositol 3-Kinases/metabolism* | - |
dc.subject.MESH | Protein Kinase Inhibitors/pharmacology | - |
dc.subject.MESH | Proto-Oncogene Proteins c-akt/agonists | - |
dc.subject.MESH | Proto-Oncogene Proteins c-akt/metabolism* | - |
dc.subject.MESH | beta Catenin/metabolism | - |
dc.title | Adherens junction-dependent PI3K/Akt activation induces resistance to genotoxin-induced cell death in differentiated intestinal epithelial cells. | - |
dc.type | Article | - |
dc.contributor.college | College of Medicine (의과대학) | - |
dc.contributor.department | Medical Research Center (임상의학연구센터) | - |
dc.contributor.googleauthor | Boah Chae | - |
dc.contributor.googleauthor | Kyoung Min Yang | - |
dc.contributor.googleauthor | Tae Il Kim | - |
dc.contributor.googleauthor | Won Ho Kim | - |
dc.identifier.doi | 10.1016/j.bbrc.2008.11.120 | - |
dc.admin.author | false | - |
dc.admin.mapping | false | - |
dc.contributor.localId | A00774 | - |
dc.contributor.localId | A01079 | - |
dc.contributor.localId | A02280 | - |
dc.contributor.localId | A04017 | - |
dc.relation.journalcode | J00281 | - |
dc.identifier.eissn | 1090-2104 | - |
dc.identifier.pmid | 19059380 | - |
dc.identifier.url | http://www.sciencedirect.com/science/article/pii/S0006291X08023073 | - |
dc.subject.keyword | Differentiation | - |
dc.subject.keyword | Cell death | - |
dc.subject.keyword | MMS | - |
dc.subject.keyword | E-cadherin | - |
dc.subject.keyword | Akt | - |
dc.contributor.alternativeName | Kim, Won Ho | - |
dc.contributor.alternativeName | Kim, Tae Il | - |
dc.contributor.alternativeName | Yang, Kyoung Min | - |
dc.contributor.alternativeName | Chae, Bo Ah | - |
dc.contributor.affiliatedAuthor | Kim, Won Ho | - |
dc.contributor.affiliatedAuthor | Kim, Tae Il | - |
dc.contributor.affiliatedAuthor | Yang, Kyoung Min | - |
dc.contributor.affiliatedAuthor | Chae, Bo Ah | - |
dc.citation.volume | 378 | - |
dc.citation.number | 4 | - |
dc.citation.startPage | 738 | - |
dc.citation.endPage | 743 | - |
dc.identifier.bibliographicCitation | BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, Vol.378(4) : 738-743, 2009 | - |
dc.identifier.rimsid | 37288 | - |
dc.type.rims | ART | - |
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