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Cited 32 times in

Expression and role of estrogen receptor α and β in medullary thyroid carcinoma: Different roles in cancer growth and apoptosis

DC FieldValueLanguage
dc.contributor.author남기현-
dc.contributor.author노태웅-
dc.contributor.author박정수-
dc.contributor.author양우익-
dc.contributor.author이유미-
dc.contributor.author이은직-
dc.contributor.author이현철-
dc.contributor.author임승길-
dc.contributor.author정웅윤-
dc.contributor.author조미애-
dc.date.accessioned2014-12-21T16:46:07Z-
dc.date.available2014-12-21T16:46:07Z-
dc.date.issued2007-
dc.identifier.issn0892-7790-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/96318-
dc.description.abstractMedullary thyroid carcinoma (MTC) originates from parafollicular C cells. Estrogen receptor beta(ERbeta) expressionwas detected in normal parafollicular C cells and MTC tumor tissue, but ERalpha expression in MTC tumors still remains undetermined. The appearance and loss of ERalpha or ERbeta expression has been known to play a role in the development and progression of many human cancers. We performed immunohistochemical studies of ERalpha, ERbeta, and Ki67, a mitotic index, in 11 human MTC tissue samples. ERalpha was detected in 10 cases (91%), and ERbeta expression was observed in 8 cases (72.7%). A majority (8/10) of ERalpha-positive tumors showing ERbeta Ki67 expression was detected in three cases (27.3%). Neither clinical parameters nor tumor node metastasis (TNM) tumor staging was correlated with the positivity for ERs or Ki67. To investigate the biological role of each ER, we used ER-negative MTC TT cells and adenoviral vectors carrying ERalpha (Ad-ERalpha), ERbeta (Ad-ERbeta), estrogen response element (ERE)-Luc (Ad-ERE-Luc), and activator protein 1 (AP1)-Luc (Ad-AP1-Luc). Estrogen stimulated and anti-estrogen, ICI 182 780, suppressed ERE reporter activity in TT cells expressing ERalpha or ERbeta, suggesting that both ERs use the same classical ERE-mediated pathway. Ad-ERalpha infection stimulated TT cell growth; in contrast, Ad-ERbeta infection suppressed their growth. Apoptosis was detected in Ad-ERbeta-infected TT cells. Estrogen and anti-estrogen suppressed AP1 activity in Ad-ERalpha-infected cells, whereas upon Ad-ERbeta infection estrogen further stimulated AP1 activity which in turn is suppressed by anti-estrogen, suggesting that each ER acts differently through a non-ERE-mediated pathway. Our results suggest that ERalpha and ERbeta may play different roles in MTC tumor growth and progression.-
dc.description.statementOfResponsibilityopen-
dc.formatapplication/pdf-
dc.relation.isPartOfJOURNAL OF ENDOUROLOGY-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.titleExpression and role of estrogen receptor α and β in medullary thyroid carcinoma: Different roles in cancer growth and apoptosis-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Pathology (병리학)-
dc.contributor.googleauthorMi Ae Cho-
dc.contributor.googleauthorMi Kyung Lee-
dc.contributor.googleauthorEun Jig Lee-
dc.contributor.googleauthorHyun Chul Lee-
dc.contributor.googleauthorSung-Kil Lim-
dc.contributor.googleauthorYumie Rhee-
dc.contributor.googleauthorWoo Ick Yang-
dc.contributor.googleauthorTaewoong Noh-
dc.contributor.googleauthorJu Hyeong Lee-
dc.contributor.googleauthorCheong Soo Park-
dc.contributor.googleauthorWoung Youn Chung-
dc.contributor.googleauthorKee-Hyun Nam-
dc.identifier.doi10.1677/JOE-06-0193-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA01245-
dc.contributor.localIdA02300-
dc.contributor.localIdA03012-
dc.contributor.localIdA03050-
dc.contributor.localIdA03301-
dc.contributor.localIdA03375-
dc.contributor.localIdA03674-
dc.contributor.localIdA03816-
dc.contributor.localIdA02768-
dc.contributor.localIdA01298-
dc.contributor.localIdA01646-
dc.relation.journalcodeJ01394-
dc.identifier.eissn1557-900X-
dc.contributor.alternativeNameNam, Kee Hyun-
dc.contributor.alternativeNameNoh, Tae Woong-
dc.contributor.alternativeNamePark, Cheong Soo-
dc.contributor.alternativeNameYang, Woo Ick-
dc.contributor.alternativeNameLee, Mi Kyung-
dc.contributor.alternativeNameRhee, Yumie-
dc.contributor.alternativeNameLee, Eun Jig-
dc.contributor.alternativeNameLee, Hyun Chul-
dc.contributor.alternativeNameLim, Sung Kil-
dc.contributor.alternativeNameChung, Woung Youn-
dc.contributor.alternativeNameCho, Mi Ae-
dc.contributor.affiliatedAuthorNam, Kee Hyun-
dc.contributor.affiliatedAuthorYang, Woo Ick-
dc.contributor.affiliatedAuthorRhee, Yumie-
dc.contributor.affiliatedAuthorLee, Eun Jig-
dc.contributor.affiliatedAuthorLee, Hyun Chul-
dc.contributor.affiliatedAuthorLim, Sung Kil-
dc.contributor.affiliatedAuthorChung, Woung Youn-
dc.contributor.affiliatedAuthorCho, Mi Ae-
dc.contributor.affiliatedAuthorLee, Mi Kyung-
dc.contributor.affiliatedAuthorNoh, Tae Woong-
dc.contributor.affiliatedAuthorPark, Cheong Soo-
dc.rights.accessRightsfree-
dc.citation.volume195-
dc.citation.number2-
dc.citation.startPage255-
dc.citation.endPage263-
dc.identifier.bibliographicCitationJOURNAL OF ENDOUROLOGY, Vol.195(2) : 255-263, 2007-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Pathology (병리학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Surgery (외과학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Internal Medicine (내과학교실) > 1. Journal Papers

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