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dc.contributor.author이영한-
dc.date.accessioned2019-07-18T02:10:42Z-
dc.date.available2019-07-18T02:10:42Z-
dc.date.issued2006-01-
dc.identifier.citationCANCER RESEARCH, v. 66, No. 2, Page. 784-793en_US
dc.identifier.issn0008-5472-
dc.identifier.issn1538-7445-
dc.identifier.urihttp://cancerres.aacrjournals.org/content/66/2/784-
dc.identifier.urihttps://repository.hanyang.ac.kr/handle/20.500.11754/107596-
dc.description.abstractPhospholipase D (PLD) has emerged as a critical regulator of cell proliferation and survival signaling. We show for the first time that elevated expression of PLD isozymes attenuates expression of the tumor suppressors early growth response-1 (Egr-1) and the phosphatase and tensin homologue deleted on chromosome 10 (PTEN) tumor suppressor and apoptosis during etoposide treatment. When formation of phosphatidic acid was inhibited by overexpression of catalytically inactive PLD during etoposide treatment, expression of Egr-1 and PTEN and the apoptotic effect of etoposide were not inhibited. This suggests that PLD inhibits expression of these tumor suppressors and inhibits apoptosis. Deletion of a specific Egr-1-binding site present in the PTEN promoter blocked etoposide-induced PTEN activity and elevated expression of PLD decreased the sensitivity to apoptosis induced by ectopic expression of Egr-1. Etoposide-induced activation of Akt was potentiated by overexpression of PLD and PLD-stimulated suppression of Egr-1 was blocked by inhibition of phosphatidylinositol 3-kinase/Akt survival pathway at the both transcriptional and posttranscriptional levels. These results show that survival signals generated by PLD attenuate expression of Egr-1 by activation of phosphatidylinositol 3-kinase signaling pathway and induction of PTEN by Egr-1, which confers resistance to apoptosis.en_US
dc.description.sponsorshipNational R&D Program for Cancer Control, Ministry of Health and Welfare, Republic of Korea, grant 0320060-2. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact. We thank Dr. Ian de Belle for providing the full-length human PTEN promoter (PTEN-luc) and its mutant constructs, Dr. I.S. Kang for providing catalytically inactive PTEN (C124S) cDNA, and Dr. Kyung Lib Jang for providing pGL2-Ecadherin and pGL2-2XSp1.en_US
dc.language.isoen_USen_US
dc.publisherAMER ASSOC CANCER RESEARCHen_US
dc.titlePhospholipase D prevents etoposide-induced apoptosis by inhibiting the expression of early growth response-1 and phosphatase and tensin homologue deleted on chromosome 10en_US
dc.typeArticleen_US
dc.identifier.doi10.1158/0008-5472.CAN-05-1316-
dc.relation.journalCANCER RESEARCH-
dc.contributor.googleauthorKim, J-
dc.contributor.googleauthorLee, YH-
dc.contributor.googleauthorKwon, TK-
dc.contributor.googleauthorChang, JS-
dc.contributor.googleauthorChung, KC-
dc.contributor.googleauthorMin, DS-
dc.relation.code2009201688-
dc.sector.campusE-
dc.sector.daehakCOLLEGE OF SCIENCE & TECHNOLOGY[E]-
dc.sector.departmentDIVISION OF MOLECULAR & LIFE SCIENCE-
dc.identifier.pidyounghan-
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COLLEGE OF SCIENCE AND CONVERGENCE TECHNOLOGY[E](과학기술융합대학) > ETC
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