Metastatic Phenotype Is Regulated by Estrogen in Thyroid Cells
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 b...
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| Veröffentlicht in: | Thyroid (New York, N.Y.) N.Y.), 2010-01, Vol.20 (1), p.33-41 |
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| creator | Rajoria, Shilpi Suriano, Robert Shanmugam, Arulkumaran Wilson, Yushan Lisa Schantz, Stimson P. Geliebter, Jan Tiwari, Raj K. |
| description | 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-α and ER-β 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 β-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. |
| doi_str_mv | 10.1089/thy.2009.0296 |
| format | Article |
| fullrecord | <record><control><sourceid>gale_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_2833180</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A217425135</galeid><sourcerecordid>A217425135</sourcerecordid><originalsourceid>FETCH-LOGICAL-c497t-a568c329a027f61cfe3c5306430ead1d69547d82a601ac5ee5bfe1da4e0b297c3</originalsourceid><addsrcrecordid>eNqFkUtLxDAURoMovpdupeC6403SJO1GkGF8gKKIrkOa3s5EOunQRKH_3gyjoiBIFgk35_tIOIScUJhQKKvzuBgnDKCaAKvkFtmnQqi8AqW20xkE5IoJuUcOQngFoLJUfJfspYBUXJX75OIeownRRGezxwX6Po4rzG5D9oTzt85EbLJ6zGYhDv0cfeZ89rwYh9412RS7LhyRndZ0AY8_90PycjV7nt7kdw_Xt9PLu9wWlYq5EbK0nFUGmGoltS1yKzjIggOahjayEoVqSmYkUGMFoqhbpI0pEGpWKcsPycWmd_VWL7Gx6ONgOr0a3NIMo-6N079vvFvoef-uWck5LSEVnG0K5qZD7XzbJ8wuXbD6klFVMEG5SNTkDyqtBpfO9h5bl-a_AvkmYIc-hAHb7ydR0Gs_OvnRaz967Sfxpz__8U1_CUkA3wDrsfG-c1jjEP-p_QDf2Jy7</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype></control><display><type>article</type><title>Metastatic Phenotype Is Regulated by Estrogen in Thyroid Cells</title><source>MEDLINE</source><source>Alma/SFX Local Collection</source><creator>Rajoria, Shilpi ; Suriano, Robert ; Shanmugam, Arulkumaran ; Wilson, Yushan Lisa ; Schantz, Stimson P. ; Geliebter, Jan ; Tiwari, Raj K.</creator><creatorcontrib>Rajoria, Shilpi ; Suriano, Robert ; Shanmugam, Arulkumaran ; Wilson, Yushan Lisa ; Schantz, Stimson P. ; Geliebter, Jan ; Tiwari, Raj K.</creatorcontrib><description>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-α and ER-β 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 β-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.</description><identifier>ISSN: 1050-7256</identifier><identifier>EISSN: 1557-9077</identifier><identifier>DOI: 10.1089/thy.2009.0296</identifier><identifier>PMID: 20067378</identifier><language>eng</language><publisher>United States: Mary Ann Liebert, Inc</publisher><subject>Analysis ; beta Catenin - metabolism ; Carcinoma, Papillary - metabolism ; Carcinoma, Papillary - pathology ; Cell Adhesion - drug effects ; Cell Line, Transformed ; Cell Line, Tumor ; Cell Movement - drug effects ; Cell Proliferation - drug effects ; Development and progression ; Down-Regulation - drug effects ; Estradiol - metabolism ; Estradiol - pharmacology ; Estrogen ; Estrogen Antagonists - pharmacology ; Estrogen Receptor alpha - metabolism ; Estrogen Receptor beta - metabolism ; Genetic aspects ; HSP90 Heat-Shock Proteins - metabolism ; Humans ; Metastasis ; Neoplasm Invasiveness ; Neoplasm Metastasis - prevention & control ; Original Studies, Reviews, and Scholarly Dialog ; Phenotype ; Physiological aspects ; Protein Transport - drug effects ; Proto-Oncogene Proteins c-akt - metabolism ; Thyroid cancer ; Thyroid Gland - drug effects ; Thyroid Gland - metabolism ; Thyroid Neoplasms - metabolism ; Thyroid Neoplasms - pathology</subject><ispartof>Thyroid (New York, N.Y.), 2010-01, Vol.20 (1), p.33-41</ispartof><rights>2009, Mary Ann Liebert, Inc.</rights><rights>COPYRIGHT 2010 Mary Ann Liebert, Inc.</rights><rights>Copyright 2010, Mary Ann Liebert, Inc.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c497t-a568c329a027f61cfe3c5306430ead1d69547d82a601ac5ee5bfe1da4e0b297c3</citedby><cites>FETCH-LOGICAL-c497t-a568c329a027f61cfe3c5306430ead1d69547d82a601ac5ee5bfe1da4e0b297c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20067378$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Rajoria, Shilpi</creatorcontrib><creatorcontrib>Suriano, Robert</creatorcontrib><creatorcontrib>Shanmugam, Arulkumaran</creatorcontrib><creatorcontrib>Wilson, Yushan Lisa</creatorcontrib><creatorcontrib>Schantz, Stimson P.</creatorcontrib><creatorcontrib>Geliebter, Jan</creatorcontrib><creatorcontrib>Tiwari, Raj K.</creatorcontrib><title>Metastatic Phenotype Is Regulated by Estrogen in Thyroid Cells</title><title>Thyroid (New York, N.Y.)</title><addtitle>Thyroid</addtitle><description>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-α and ER-β 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 β-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.</description><subject>Analysis</subject><subject>beta Catenin - metabolism</subject><subject>Carcinoma, Papillary - metabolism</subject><subject>Carcinoma, Papillary - pathology</subject><subject>Cell Adhesion - drug effects</subject><subject>Cell Line, Transformed</subject><subject>Cell Line, Tumor</subject><subject>Cell Movement - drug effects</subject><subject>Cell Proliferation - drug effects</subject><subject>Development and progression</subject><subject>Down-Regulation - drug effects</subject><subject>Estradiol - metabolism</subject><subject>Estradiol - pharmacology</subject><subject>Estrogen</subject><subject>Estrogen Antagonists - pharmacology</subject><subject>Estrogen Receptor alpha - metabolism</subject><subject>Estrogen Receptor beta - metabolism</subject><subject>Genetic aspects</subject><subject>HSP90 Heat-Shock Proteins - metabolism</subject><subject>Humans</subject><subject>Metastasis</subject><subject>Neoplasm Invasiveness</subject><subject>Neoplasm Metastasis - prevention & control</subject><subject>Original Studies, Reviews, and Scholarly Dialog</subject><subject>Phenotype</subject><subject>Physiological aspects</subject><subject>Protein Transport - drug effects</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>Thyroid cancer</subject><subject>Thyroid Gland - drug effects</subject><subject>Thyroid Gland - metabolism</subject><subject>Thyroid Neoplasms - metabolism</subject><subject>Thyroid Neoplasms - pathology</subject><issn>1050-7256</issn><issn>1557-9077</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkUtLxDAURoMovpdupeC6403SJO1GkGF8gKKIrkOa3s5EOunQRKH_3gyjoiBIFgk35_tIOIScUJhQKKvzuBgnDKCaAKvkFtmnQqi8AqW20xkE5IoJuUcOQngFoLJUfJfspYBUXJX75OIeownRRGezxwX6Po4rzG5D9oTzt85EbLJ6zGYhDv0cfeZ89rwYh9412RS7LhyRndZ0AY8_90PycjV7nt7kdw_Xt9PLu9wWlYq5EbK0nFUGmGoltS1yKzjIggOahjayEoVqSmYkUGMFoqhbpI0pEGpWKcsPycWmd_VWL7Gx6ONgOr0a3NIMo-6N079vvFvoef-uWck5LSEVnG0K5qZD7XzbJ8wuXbD6klFVMEG5SNTkDyqtBpfO9h5bl-a_AvkmYIc-hAHb7ydR0Gs_OvnRaz967Sfxpz__8U1_CUkA3wDrsfG-c1jjEP-p_QDf2Jy7</recordid><startdate>20100101</startdate><enddate>20100101</enddate><creator>Rajoria, Shilpi</creator><creator>Suriano, Robert</creator><creator>Shanmugam, Arulkumaran</creator><creator>Wilson, Yushan Lisa</creator><creator>Schantz, Stimson P.</creator><creator>Geliebter, Jan</creator><creator>Tiwari, Raj K.</creator><general>Mary Ann Liebert, Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>5PM</scope></search><sort><creationdate>20100101</creationdate><title>Metastatic Phenotype Is Regulated by Estrogen in Thyroid Cells</title><author>Rajoria, Shilpi ; Suriano, Robert ; Shanmugam, Arulkumaran ; Wilson, Yushan Lisa ; Schantz, Stimson P. ; Geliebter, Jan ; Tiwari, Raj K.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c497t-a568c329a027f61cfe3c5306430ead1d69547d82a601ac5ee5bfe1da4e0b297c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>Analysis</topic><topic>beta Catenin - metabolism</topic><topic>Carcinoma, Papillary - metabolism</topic><topic>Carcinoma, Papillary - pathology</topic><topic>Cell Adhesion - drug effects</topic><topic>Cell Line, Transformed</topic><topic>Cell Line, Tumor</topic><topic>Cell Movement - drug effects</topic><topic>Cell Proliferation - drug effects</topic><topic>Development and progression</topic><topic>Down-Regulation - drug effects</topic><topic>Estradiol - metabolism</topic><topic>Estradiol - pharmacology</topic><topic>Estrogen</topic><topic>Estrogen Antagonists - pharmacology</topic><topic>Estrogen Receptor alpha - metabolism</topic><topic>Estrogen Receptor beta - metabolism</topic><topic>Genetic aspects</topic><topic>HSP90 Heat-Shock Proteins - metabolism</topic><topic>Humans</topic><topic>Metastasis</topic><topic>Neoplasm Invasiveness</topic><topic>Neoplasm Metastasis - prevention & control</topic><topic>Original Studies, Reviews, and Scholarly Dialog</topic><topic>Phenotype</topic><topic>Physiological aspects</topic><topic>Protein Transport - drug effects</topic><topic>Proto-Oncogene Proteins c-akt - metabolism</topic><topic>Thyroid cancer</topic><topic>Thyroid Gland - drug effects</topic><topic>Thyroid Gland - metabolism</topic><topic>Thyroid Neoplasms - metabolism</topic><topic>Thyroid Neoplasms - pathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Rajoria, Shilpi</creatorcontrib><creatorcontrib>Suriano, Robert</creatorcontrib><creatorcontrib>Shanmugam, Arulkumaran</creatorcontrib><creatorcontrib>Wilson, Yushan Lisa</creatorcontrib><creatorcontrib>Schantz, Stimson P.</creatorcontrib><creatorcontrib>Geliebter, Jan</creatorcontrib><creatorcontrib>Tiwari, Raj K.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Thyroid (New York, N.Y.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Rajoria, Shilpi</au><au>Suriano, Robert</au><au>Shanmugam, Arulkumaran</au><au>Wilson, Yushan Lisa</au><au>Schantz, Stimson P.</au><au>Geliebter, Jan</au><au>Tiwari, Raj K.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Metastatic Phenotype Is Regulated by Estrogen in Thyroid Cells</atitle><jtitle>Thyroid (New York, N.Y.)</jtitle><addtitle>Thyroid</addtitle><date>2010-01-01</date><risdate>2010</risdate><volume>20</volume><issue>1</issue><spage>33</spage><epage>41</epage><pages>33-41</pages><issn>1050-7256</issn><eissn>1557-9077</eissn><abstract>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-α and ER-β 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 β-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.</abstract><cop>United States</cop><pub>Mary Ann Liebert, Inc</pub><pmid>20067378</pmid><doi>10.1089/thy.2009.0296</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1050-7256 |
| ispartof | Thyroid (New York, N.Y.), 2010-01, Vol.20 (1), p.33-41 |
| issn | 1050-7256 1557-9077 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_2833180 |
| source | MEDLINE; Alma/SFX Local Collection |
| subjects | Analysis beta Catenin - metabolism Carcinoma, Papillary - metabolism Carcinoma, Papillary - pathology Cell Adhesion - drug effects Cell Line, Transformed Cell Line, Tumor Cell Movement - drug effects Cell Proliferation - drug effects Development and progression Down-Regulation - drug effects Estradiol - metabolism Estradiol - pharmacology Estrogen Estrogen Antagonists - pharmacology Estrogen Receptor alpha - metabolism Estrogen Receptor beta - metabolism Genetic aspects HSP90 Heat-Shock Proteins - metabolism Humans Metastasis Neoplasm Invasiveness Neoplasm Metastasis - prevention & control Original Studies, Reviews, and Scholarly Dialog Phenotype Physiological aspects Protein Transport - drug effects Proto-Oncogene Proteins c-akt - metabolism Thyroid cancer Thyroid Gland - drug effects Thyroid Gland - metabolism Thyroid Neoplasms - metabolism Thyroid Neoplasms - pathology |
| title | Metastatic Phenotype Is Regulated by Estrogen in Thyroid Cells |
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