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

Authors
 Mi Ae Cho  ;  Mi Kyung Lee  ;  Eun Jig Lee  ;  Hyun Chul Lee  ;  Sung-Kil Lim  ;  Yumie Rhee  ;  Woo Ick Yang  ;  Taewoong Noh  ;  Ju Hyeong Lee  ;  Cheong Soo Park  ;  Woung Youn Chung  ;  Kee-Hyun Nam 
Citation
 JOURNAL OF ENDOUROLOGY, Vol.195(2) : 255-263, 2007 
Journal Title
 JOURNAL OF ENDOUROLOGY 
ISSN
 0892-7790 
Issue Date
2007
Abstract
Medullary 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.
Files in This Item:
T200700546.pdf Download
DOI
10.1677/JOE-06-0193
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
Yonsei Authors
Nam, Kee Hyun(남기현) ORCID logo https://orcid.org/0000-0002-6852-1190
Noh, Tae Woong(노태웅)
Park, Cheong Soo(박정수)
Yang, Woo Ick(양우익) ORCID logo https://orcid.org/0000-0002-6084-5019
Rhee, Yumie(이유미) ORCID logo https://orcid.org/0000-0003-4227-5638
Lee, Eun Jig(이은직) ORCID logo https://orcid.org/0000-0002-9876-8370
Lee, Hyun Chul(이현철)
Lim, Sung Kil(임승길)
Chung, Woong Youn(정웅윤)
Cho, Mi Ae(조미애)
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/96318
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