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Low-concentration vemurafenib induces the proliferation and invasion of human HaCaT keratinocytes through mitogen-activated protein kinase pathway activation

DC FieldValueLanguage
dc.contributor.author노미령-
dc.contributor.author라선영-
dc.contributor.author이상희-
dc.contributor.author정기양-
dc.date.accessioned2016-02-04T11:47:11Z-
dc.date.available2016-02-04T11:47:11Z-
dc.date.issued2015-
dc.identifier.issn0385-2407-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/141199-
dc.description.abstractCutaneous squamous cell carcinomas and keratoacanthomas commonly occur in patients treated with BRAF inhibitors. We investigated the effect of the BRAF inhibitor vemurafenib on normal immortalized human HaCaT keratinocytes to explore the mechanism of hyperproliferative cutaneous neoplasia associated with the use of BRAF inhibitors. Vemurafenib induced an increase in viable cell number in BRAF wild-type cell lines (SK-MEL-2 and HaCaT) but not in BRAF mutant cell lines (SK-MEL-24 and G361). In HaCaT keratinocytes, a low concentration (2 μmol/L) of vemurafenib increased cell proliferation and activated mitogen-activated protein kinase kinase/extracellular signal-regulated kinase in a CRAF-dependent manner. Invasiveness of HaCaT cells in a Matrigel assay significantly increased upon cultivation of cells with 2 μmol/L vemurafenib for 24 h. Gelatin zymography, reverse transcription polymerase chain reaction and western blot results revealed that 2 μmol/L vemurafenib treatment increased matrix metalloproteinase (MMP)-2 and MMP-9 expressions and activities in HaCaT cells. These results offer additional insight into the complex mechanism of paradoxical mitogen-activated protein kinase signaling involved in hyperproliferative cutaneous neoplasias that arise after BRAF inhibition and suggest a possible role for MMP in tumor progression and invasion.-
dc.description.statementOfResponsibilityopen-
dc.format.extent881~888-
dc.relation.isPartOfJournal of Dermatology-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.titleLow-concentration vemurafenib induces the proliferation and invasion of human HaCaT keratinocytes through mitogen-activated protein kinase pathway activation-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Internal Medicine (내과학)-
dc.contributor.googleauthorMi Ryung Roh-
dc.contributor.googleauthorJung Min Kim-
dc.contributor.googleauthorSang Hee Lee-
dc.contributor.googleauthorHong Sun Jang-
dc.contributor.googleauthorKyu Hyun Park-
dc.contributor.googleauthorKee Yang Chung-
dc.contributor.googleauthorSun Young Rha-
dc.identifier.doi10.1111/1346-8138.12950-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA01278-
dc.contributor.localIdA03582-
dc.contributor.localIdA01316-
dc.contributor.localIdA02841-
dc.relation.journalcodeJ01372-
dc.identifier.urlhttp://onlinelibrary.wiley.com/doi/10.1111/1346-8138.12950/abstract-
dc.contributor.alternativeNameRoh, Mi Ryung-
dc.contributor.alternativeNameRha, Sun Young-
dc.contributor.alternativeNameLee, Sang Hee-
dc.contributor.alternativeNameChung, Kee Yang-
dc.contributor.affiliatedAuthorRoh, Mi Ryung-
dc.contributor.affiliatedAuthorChung, Kee Yang-
dc.contributor.affiliatedAuthorRha, Sun Young-
dc.contributor.affiliatedAuthorLee, Sang Hee-
dc.rights.accessRightsnot free-
dc.citation.volume42-
dc.citation.number9-
dc.citation.startPage881-
dc.citation.endPage888-
dc.identifier.bibliographicCitationJournal of Dermatology, Vol.42(9) : 881-888, 2015-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Internal Medicine (내과학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Dermatology (피부과학교실) > 1. Journal Papers

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