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Up-regulation of acetyl-CoA carboxylase α and fatty acid synthase by human epidermal growth factor receptor 2 at the translational level in breast cancer cells

DC Field Value Language
dc.contributor.author고유경-
dc.contributor.author김경섭-
dc.contributor.author박병우-
dc.contributor.author박상욱-
dc.contributor.author안용호-
dc.contributor.author윤사라-
dc.contributor.author이민영-
dc.date.accessioned2014-12-21T16:43:09Z-
dc.date.available2014-12-21T16:43:09Z-
dc.date.issued2007-
dc.identifier.issn0021-9258-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/96221-
dc.description.abstractExpression of the HER2 oncogene is increased in ∼30% of human breast carcinomas and is closely correlated with the expression of fatty acid synthase (FASN). In the present study, we determined the mechanism by which FASN and acetyl-CoA carboxylase α (ACCα) could be induced by HER2 overexpression. SK-BR-3 and BT-474 cells, breast cancer cells that overexpress HER2, expressed higher levels of FASN and ACCα compared with MCF-7 and MDA-MB-231 breast cancer cells in which HER2 expression is low. The induction of FASN and ACCα in BT474 cells were not mediated by the activation of SREBP-1. Exogenous HER2 expression in MDA-MB-231 cells induced the expression of FASN and ACCα, and the HER2-mediated increase in ACCα and FASN was inhibited by both LY294002, a phosphatidylinositol 3-kinase inhibitor, and rapamycin, a mammalian target of rapamycin (mTOR) inhibitor. In addition, the activation of mTOR by the overexpression of RHEB in MDA-MB-231 cells increased the synthetic rates of both FASN and ACCα. On the other hand, FASN and ACCα were reduced in BT-474 cells by a blockade of the mTOR signaling pathway. These changes observed in their protein levels were not accompanied by changes in their mRNA levels. The 5′- and 3′-untranslated regions of both FASN and ACCα mRNAs were involved in selective translational induction that was mediated by mTOR signal transduction. These results strongly suggest that the major mechanism of HER2-mediated induction of FASN and ACCα in the breast cancer cells used in this study is translational regulation primarily through the mTOR signaling pathway.-
dc.description.statementOfResponsibilityopen-
dc.format.extent26122~26131-
dc.relation.isPartOfJOURNAL OF BIOLOGICAL CHEMISTRY-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.subject.MESH3' Untranslated Regions/genetics-
dc.subject.MESH3' Untranslated Regions/metabolism-
dc.subject.MESH5' Untranslated Regions/genetics-
dc.subject.MESH5' Untranslated Regions/metabolism-
dc.subject.MESHAcetyl-CoA Carboxylase/biosynthesis*-
dc.subject.MESHAcetyl-CoA Carboxylase/genetics-
dc.subject.MESHBreast Neoplasms/enzymology*-
dc.subject.MESHBreast Neoplasms/genetics-
dc.subject.MESHCell Line, Tumor-
dc.subject.MESHChromones/pharmacology-
dc.subject.MESHEnzyme Induction/drug effects-
dc.subject.MESHEnzyme Inhibitors/pharmacology-
dc.subject.MESHErbB Receptors/genetics-
dc.subject.MESHErbB Receptors/metabolism-
dc.subject.MESHFatty Acid Synthases/biosynthesis*-
dc.subject.MESHFatty Acid Synthases/genetics-
dc.subject.MESHFemale-
dc.subject.MESHGene Expression Regulation, Neoplastic*/drug effects-
dc.subject.MESHHumans-
dc.subject.MESHMorpholines/pharmacology-
dc.subject.MESHPhosphatidylinositol 3-Kinases/antagonists & inhibitors-
dc.subject.MESHPhosphatidylinositol 3-Kinases/metabolism-
dc.subject.MESHProtein Biosynthesis*/drug effects-
dc.subject.MESHProtein Kinases/metabolism-
dc.subject.MESHRNA, Neoplasm/genetics-
dc.subject.MESHRNA, Neoplasm/metabolism-
dc.subject.MESHReceptor, ErbB-2/genetics-
dc.subject.MESHReceptor, ErbB-2/metabolism*-
dc.subject.MESHSignal Transduction*/drug effects-
dc.subject.MESHSterol Regulatory Element Binding Protein 1/genetics-
dc.subject.MESHSterol Regulatory Element Binding Protein 1/metabolism-
dc.subject.MESHTOR Serine-Threonine Kinases-
dc.titleUp-regulation of acetyl-CoA carboxylase α and fatty acid synthase by human epidermal growth factor receptor 2 at the translational level in breast cancer cells-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Biochemistry & Molecular Biology (생화학,분자생물학)-
dc.contributor.googleauthorSarah Yoon-
dc.contributor.googleauthorMin-Young Lee-
dc.contributor.googleauthorKyung-Sup Kim-
dc.contributor.googleauthorByeong-Woo Park-
dc.contributor.googleauthorYong-Ho Ahn-
dc.contributor.googleauthorYoo-Kyung Koh-
dc.contributor.googleauthorJong-Seok Moon-
dc.contributor.googleauthorSahng Wook Park-
dc.identifier.doi10.1074/jbc.M702854200-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA00132-
dc.contributor.localIdA00297-
dc.contributor.localIdA01475-
dc.contributor.localIdA01487-
dc.contributor.localIdA02249-
dc.contributor.localIdA02557-
dc.contributor.localIdA02783-
dc.relation.journalcodeJ01258-
dc.identifier.eissn1083-351X-
dc.identifier.pmid17631500-
dc.contributor.alternativeNameKoh, Yoo Kyung-
dc.contributor.alternativeNameKim, Kyung Sup-
dc.contributor.alternativeNamePark, Byeong Woo-
dc.contributor.alternativeNamePark, Sahng Wook-
dc.contributor.alternativeNameAhn, Yong Ho-
dc.contributor.alternativeNameYoon, Sa Rah-
dc.contributor.alternativeNameLee, Min Young-
dc.contributor.affiliatedAuthorKoh, Yoo Kyung-
dc.contributor.affiliatedAuthorKim, Kyung Sup-
dc.contributor.affiliatedAuthorPark, Byeong Woo-
dc.contributor.affiliatedAuthorPark, Sahng Wook-
dc.contributor.affiliatedAuthorAhn, Yong Ho-
dc.contributor.affiliatedAuthorYoon, Sa Rah-
dc.contributor.affiliatedAuthorLee, Min Young-
dc.rights.accessRightsfree-
dc.citation.volume282-
dc.citation.number36-
dc.citation.startPage26122-
dc.citation.endPage26131-
dc.identifier.bibliographicCitationJOURNAL OF BIOLOGICAL CHEMISTRY, Vol.282(36) : 26122-26131, 2007-
dc.identifier.rimsid34987-
dc.type.rimsART-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Biochemistry and Molecular Biology (생화학-분자생물학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Surgery (외과학교실) > 1. Journal Papers

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