| Metastatic phenotype is regulated by estrogen in thyroid cells. | |
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MedLine Citation:
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PMID: 20067378 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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BACKGROUND: Over 200 million people worldwide are affected by thyroid proliferative diseases, including cancer, adenoma, and goiter, annually. The incidences of thyroid malignancies are three to four times higher in women, suggesting the possible involvement of estrogen. Based on this observed sex bias, we hypothesize that estrogen modulates the growth and metastatic propensity of thyroid cancer cells. METHODS: In this study, two thyroid cell lines (Nthy-ori 3-1 and BCPAP) were evaluated for the presence of estrogen receptor (ER) by Western blot analysis and estrogen responsiveness by using a cell proliferation assay. In addition, the effect of estradiol (E(2)) on modulation of metastatic phenotype was determined by using in vitro adhesion, migration, and invasion assays. RESULTS: Thyroid cells expressed a functionally active ER-alpha and ER-beta as evidenced by 50-150% enhancement of proliferation in the presence of E(2). E(2) also enhanced adhesion, migration, and invasion of thyroid cells in an in vitro experimental model system that, based on our results, is modulated by beta-catenin. CONCLUSION: Our data provide evidence that the higher incidence of thyroid cancer in women is potentially attributed to the presence of a functional ER that participates in cellular processes contributing to enhanced mitogenic, migratory, and invasive properties of thyroid cells. These findings will enable and foster the possible development of antiestrogenic therapy targeting invasion and migration, thus affecting metastatic propensity. |
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Authors:
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Shilpi Rajoria; Robert Suriano; Arulkumaran Shanmugam; Yushan Lisa Wilson; Stimson P Schantz; Jan Geliebter; Raj K Tiwari |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: Thyroid : official journal of the American Thyroid Association Volume: 20 ISSN: 1557-9077 ISO Abbreviation: Thyroid Publication Date: 2010 Jan |
Date Detail:
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Created Date: 2010-01-13 Completed Date: 2010-04-08 Revised Date: 2013-04-12 |
Medline Journal Info:
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Nlm Unique ID: 9104317 Medline TA: Thyroid Country: United States |
Other Details:
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Languages: eng Pagination: 33-41 Citation Subset: IM |
Affiliation:
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Department of Microbiology and Immunology, New York Medical College, Valhalla, New York 10595, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Carcinoma, Papillary
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metabolism,
pathology Cell Adhesion / drug effects Cell Line, Transformed Cell Line, Tumor Cell Movement / drug effects Cell Proliferation / drug effects Down-Regulation / drug effects Estradiol / metabolism, pharmacology* Estrogen Antagonists / pharmacology Estrogen Receptor alpha / metabolism* Estrogen Receptor beta / metabolism* HSP90 Heat-Shock Proteins / metabolism Humans Neoplasm Invasiveness Neoplasm Metastasis* / prevention & control Phenotype Protein Transport / drug effects Proto-Oncogene Proteins c-akt / metabolism Thyroid Gland / drug effects, metabolism Thyroid Neoplasms / metabolism*, pathology* beta Catenin / metabolism |
| Grant Support | |
ID/Acronym/Agency:
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1R01CA131946-01A2/CA/NCI NIH HHS; R01 CA131946/CA/NCI NIH HHS; R01 CA131946-01A2/CA/NCI NIH HHS; R01 CA131946-02/CA/NCI NIH HHS; R01 CA131946-03/CA/NCI NIH HHS; R01 CA131946-04/CA/NCI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Estrogen Antagonists; 0/Estrogen Receptor alpha; 0/Estrogen Receptor beta; 0/HSP90 Heat-Shock Proteins; 0/beta Catenin; 50-28-2/Estradiol; EC 2.7.11.1/Proto-Oncogene Proteins c-akt |
| Comments/Corrections | |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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