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STAT3 is involved in phosphatidic acid-induced Bcl-2 expression in HeLa cells

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dc.contributor.authorChoi, Hye-Jin-
dc.contributor.authorLee, Jung Han-
dc.contributor.authorPark, Shin-Young-
dc.contributor.authorCho, Ju Hwan-
dc.contributor.authorHan, Joong-Soo-
dc.date.accessioned2022-12-20T23:41:07Z-
dc.date.available2022-12-20T23:41:07Z-
dc.date.created2022-08-26-
dc.date.issued2009-02-
dc.identifier.issn1226-3613-
dc.identifier.urihttps://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/177342-
dc.description.abstractPhosphatidic acid (PA), the product of a PLD-mediated reaction, is a lipid second messenger that participates in various intracellular signaling events and is known to regulate a growing list of signaling proteins. We found that Bcl-2 was upregulated by PA treatment in HeLa cells. However, how PA upregulates Bcl-2 expression has not yet been studied. In this study, we tried to discover the mechanisms of Bcl-2 up-regulation by PA treatment in HeLa cells. Treatment with PA resulted in significantly increased expression of Bcl-2 in HeLa cells. Moreover, PA-induced Bcl-2 expression was blocked by mepacrine, an inhibitor of PLA(2), but not by propranolol, an inhibitor of PA phospholyhydrolase (PAP). Treatment of 1,2-dipalmitoryl-sn-glycero-3-phosphate (DPPA) also increased Bcl-2 expression. These results indicate that Bcl-2 expression is mediated by lysophosphatidic acid (LPA), not by arachidonic acid (AA). Thereafter, we used MEK1/2 inhibitor, PD98059 to investigate the relationship between ERK1/2 MAPK and PA-induced Bcl-2 expression. PA-induced Bcl-2 expression was decreased when ERK1/2 was inhibited by PD98059. The transcription factor such as STAT3 which is controlled by ERK1/2 MAPK was increased along with Bcl-2 expression when the cells were treated with PA. Furthermore, STAT3 siRNA treatments inhibited PA-induced Bcl-2 expression, suggesting that STAT3 (Ser(727)) is involved in PA-induced Bcl-2 expression. Taken together, these findings indicate that PA acts as an important mediator for increasing Bcl-2 expression through STAT3 (Ser(727)) activation via the ERK1/2 MAPK pathway.-
dc.language영어-
dc.language.isoen-
dc.publisherSPRINGERNATURE-
dc.titleSTAT3 is involved in phosphatidic acid-induced Bcl-2 expression in HeLa cells-
dc.typeArticle-
dc.contributor.affiliatedAuthorHan, Joong-Soo-
dc.identifier.doi10.3858/emm.2009.41.2.012-
dc.identifier.scopusid2-s2.0-63849342104-
dc.identifier.wosid000263896200005-
dc.identifier.bibliographicCitationEXPERIMENTAL AND MOLECULAR MEDICINE, v.41, no.2, pp.94 - 101-
dc.relation.isPartOfEXPERIMENTAL AND MOLECULAR MEDICINE-
dc.citation.titleEXPERIMENTAL AND MOLECULAR MEDICINE-
dc.citation.volume41-
dc.citation.number2-
dc.citation.startPage94-
dc.citation.endPage101-
dc.type.rimsART-
dc.type.docTypeArticle-
dc.identifier.kciidART001318534-
dc.description.journalClass1-
dc.description.isOpenAccessY-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.description.journalRegisteredClasskci-
dc.relation.journalResearchAreaBiochemistry & Molecular Biology-
dc.relation.journalResearchAreaResearch & Experimental Medicine-
dc.relation.journalWebOfScienceCategoryBiochemistry & Molecular Biology-
dc.relation.journalWebOfScienceCategoryMedicine, Research & Experimental-
dc.subject.keywordPlusSERINE PHOSPHORYLATION-
dc.subject.keywordPlusCANCER CELLS-
dc.subject.keywordPlusTRANSCRIPTIONAL ACTIVITY-
dc.subject.keywordPlusMAXIMAL ACTIVATION-
dc.subject.keywordPlusPROMOTES SURVIVAL-
dc.subject.keywordPlusINDUCED APOPTOSIS-
dc.subject.keywordPlusPROTEIN FAMILY-
dc.subject.keywordPlusDEATH-
dc.subject.keywordPlusPATHWAY-
dc.subject.keywordPlusMITOCHONDRIA-
dc.subject.keywordAuthorextracellular signal-regulated MAP kinases-
dc.subject.keywordAuthorphosphatidic acids-
dc.subject.keywordAuthorphospholipases A2-
dc.subject.keywordAuthorproto-oncogene proteins c-bcl-2-
dc.subject.keywordAuthorSTAT3 transcription factor-
dc.identifier.urlhttps://www.nature.com/articles/emm200913-
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