| Autor: |
Cho MA; Division of Endocrinology, Yonsei University College of Medicine, Seoul, South Korea., Lee MK, Nam KH, Chung WY, Park CS, Lee JH, Noh T, Yang WI, Rhee Y, Lim SK, Lee HC, Lee EJ |
| Jazyk: |
angličtina |
| Zdroj: |
The Journal of endocrinology [J Endocrinol] 2007 Nov; Vol. 195 (2), pp. 255-63. |
| DOI: |
10.1677/JOE-06-0193 |
| Abstrakt: |
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. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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