Down-regulation of NR4A1 in follicular thyroid carcinomas is restored following lithium treatment
Summary Introduction The identification of follicular thyroid adenoma‐associated transcripts will lead to a better understanding of the events involved in pathogenesis and progression of follicular tumours. Using Serial Analysis of Gene Expression, we identified five genes that are absent in a mali...
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| Veröffentlicht in: | Clinical endocrinology (Oxford) 2009-03, Vol.70 (3), p.475-483 |
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| creator | Camacho, Cléber P. Latini, Flavia R. M. Oler, Gisele Hojaij, Flavio C. Maciel, Rui M. B. Riggins, Gregory J. Cerutti, Janete M. |
| description | Summary
Introduction The identification of follicular thyroid adenoma‐associated transcripts will lead to a better understanding of the events involved in pathogenesis and progression of follicular tumours. Using Serial Analysis of Gene Expression, we identified five genes that are absent in a malignant follicular thyroid carcinoma (FTC) library, but expressed in follicular adenoma (FTA) and normal thyroid libraries.
Methods NR4A1, one of the five genes, was validated in a set of 27 normal thyroid tissues, 10 FTAs and 14 FTCs and three thyroid carcinoma cell lines by real time PCR. NR4A1 can be transiently increased by a variety of stimuli, including lithium, which is used as adjuvant therapy of thyroid carcinoma with 131I. We tested if lithium could restore NR4A1 expression. The expression of other genes potentially involved in the same signalling pathway was tested. To this end, lithium was used at different concentration (10 mm or 20 mm) and time (2 h and 24 h) and the level of expression was tested by quantitative PCR. We next tested if Lithium could affect cell growth and apoptosis.
Results We observed that NR4A1 expression was under‐expressed in most of the FTCs investigated, compared with expression in normal thyroid tissues and FTAs. We also found a positive correlation between NR4A1 and FOSB gene expression. Lithium induced NR4A1 and FOSB expression, reduced CCDN1 expression, inhibited cell growth and triggered apoptosis in a FTC cell line.
Conclusions NR4A1 is under‐expressed in most of FTCs. The loss of expression of both NR4A1 and the Wnt pathway gene FOSB was correlated with malignancy. This is consistent with the hypothesis that its loss of expression is part of the transformation process of FTCs, either as a direct or indirect consequence of Wnt pathway alterations. Lithium restores NR4A1 expression, induces apoptosis and reduces cell growth. These findings may explain a possible molecular mechanism of lithium's therapeutic action. |
| doi_str_mv | 10.1111/j.1365-2265.2008.03349.x |
| format | Article |
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Introduction The identification of follicular thyroid adenoma‐associated transcripts will lead to a better understanding of the events involved in pathogenesis and progression of follicular tumours. Using Serial Analysis of Gene Expression, we identified five genes that are absent in a malignant follicular thyroid carcinoma (FTC) library, but expressed in follicular adenoma (FTA) and normal thyroid libraries.
Methods NR4A1, one of the five genes, was validated in a set of 27 normal thyroid tissues, 10 FTAs and 14 FTCs and three thyroid carcinoma cell lines by real time PCR. NR4A1 can be transiently increased by a variety of stimuli, including lithium, which is used as adjuvant therapy of thyroid carcinoma with 131I. We tested if lithium could restore NR4A1 expression. The expression of other genes potentially involved in the same signalling pathway was tested. To this end, lithium was used at different concentration (10 mm or 20 mm) and time (2 h and 24 h) and the level of expression was tested by quantitative PCR. We next tested if Lithium could affect cell growth and apoptosis.
Results We observed that NR4A1 expression was under‐expressed in most of the FTCs investigated, compared with expression in normal thyroid tissues and FTAs. We also found a positive correlation between NR4A1 and FOSB gene expression. Lithium induced NR4A1 and FOSB expression, reduced CCDN1 expression, inhibited cell growth and triggered apoptosis in a FTC cell line.
Conclusions NR4A1 is under‐expressed in most of FTCs. The loss of expression of both NR4A1 and the Wnt pathway gene FOSB was correlated with malignancy. This is consistent with the hypothesis that its loss of expression is part of the transformation process of FTCs, either as a direct or indirect consequence of Wnt pathway alterations. Lithium restores NR4A1 expression, induces apoptosis and reduces cell growth. These findings may explain a possible molecular mechanism of lithium's therapeutic action.</description><identifier>ISSN: 0300-0664</identifier><identifier>EISSN: 1365-2265</identifier><identifier>DOI: 10.1111/j.1365-2265.2008.03349.x</identifier><identifier>PMID: 18727708</identifier><identifier>CODEN: CLECAP</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Adenocarcinoma, Follicular - drug therapy ; Adenocarcinoma, Follicular - metabolism ; Adenocarcinoma, Follicular - pathology ; Adenoma - drug therapy ; Adenoma - metabolism ; Adenoma - pathology ; Apoptosis - drug effects ; Biological and medical sciences ; Cell Line, Tumor ; Cell Proliferation - drug effects ; Chemotherapy, Adjuvant ; Cyclin D1 - genetics ; Cyclin D1 - metabolism ; DNA-Binding Proteins - genetics ; DNA-Binding Proteins - metabolism ; Dose-Response Relationship, Drug ; Down-Regulation - drug effects ; Endocrinopathies ; Fundamental and applied biological sciences. Psychology ; Humans ; Lithium Compounds - pharmacology ; Lithium Compounds - therapeutic use ; Malignant tumors ; Medical sciences ; Non tumoral diseases. Target tissue resistance. Benign neoplasms ; Nuclear Receptor Subfamily 4, Group A, Member 1 ; Proto-Oncogene Proteins c-fos - genetics ; Proto-Oncogene Proteins c-fos - metabolism ; Receptors, Steroid - genetics ; Receptors, Steroid - metabolism ; Signal Transduction - drug effects ; Thyroid Neoplasms - drug therapy ; Thyroid Neoplasms - metabolism ; Thyroid Neoplasms - pathology ; Thyroid. Thyroid axis (diseases) ; Vertebrates: endocrinology ; Wnt Proteins - genetics ; Wnt Proteins - metabolism</subject><ispartof>Clinical endocrinology (Oxford), 2009-03, Vol.70 (3), p.475-483</ispartof><rights>2009 The Authors. Journal compilation © 2009 Blackwell Publishing Ltd</rights><rights>2009 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5409-5e7942d9da88eec74e5ceb3e5dc9fb39f6dbeb23efe9afc0fe930ac2e6a3de8f3</citedby><cites>FETCH-LOGICAL-c5409-5e7942d9da88eec74e5ceb3e5dc9fb39f6dbeb23efe9afc0fe930ac2e6a3de8f3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fj.1365-2265.2008.03349.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fj.1365-2265.2008.03349.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>230,314,777,781,882,1412,27905,27906,45555,45556</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=21139266$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18727708$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Camacho, Cléber P.</creatorcontrib><creatorcontrib>Latini, Flavia R. M.</creatorcontrib><creatorcontrib>Oler, Gisele</creatorcontrib><creatorcontrib>Hojaij, Flavio C.</creatorcontrib><creatorcontrib>Maciel, Rui M. B.</creatorcontrib><creatorcontrib>Riggins, Gregory J.</creatorcontrib><creatorcontrib>Cerutti, Janete M.</creatorcontrib><title>Down-regulation of NR4A1 in follicular thyroid carcinomas is restored following lithium treatment</title><title>Clinical endocrinology (Oxford)</title><addtitle>Clin Endocrinol (Oxf)</addtitle><description>Summary
Introduction The identification of follicular thyroid adenoma‐associated transcripts will lead to a better understanding of the events involved in pathogenesis and progression of follicular tumours. Using Serial Analysis of Gene Expression, we identified five genes that are absent in a malignant follicular thyroid carcinoma (FTC) library, but expressed in follicular adenoma (FTA) and normal thyroid libraries.
Methods NR4A1, one of the five genes, was validated in a set of 27 normal thyroid tissues, 10 FTAs and 14 FTCs and three thyroid carcinoma cell lines by real time PCR. NR4A1 can be transiently increased by a variety of stimuli, including lithium, which is used as adjuvant therapy of thyroid carcinoma with 131I. We tested if lithium could restore NR4A1 expression. The expression of other genes potentially involved in the same signalling pathway was tested. To this end, lithium was used at different concentration (10 mm or 20 mm) and time (2 h and 24 h) and the level of expression was tested by quantitative PCR. We next tested if Lithium could affect cell growth and apoptosis.
Results We observed that NR4A1 expression was under‐expressed in most of the FTCs investigated, compared with expression in normal thyroid tissues and FTAs. We also found a positive correlation between NR4A1 and FOSB gene expression. Lithium induced NR4A1 and FOSB expression, reduced CCDN1 expression, inhibited cell growth and triggered apoptosis in a FTC cell line.
Conclusions NR4A1 is under‐expressed in most of FTCs. The loss of expression of both NR4A1 and the Wnt pathway gene FOSB was correlated with malignancy. This is consistent with the hypothesis that its loss of expression is part of the transformation process of FTCs, either as a direct or indirect consequence of Wnt pathway alterations. Lithium restores NR4A1 expression, induces apoptosis and reduces cell growth. These findings may explain a possible molecular mechanism of lithium's therapeutic action.</description><subject>Adenocarcinoma, Follicular - drug therapy</subject><subject>Adenocarcinoma, Follicular - metabolism</subject><subject>Adenocarcinoma, Follicular - pathology</subject><subject>Adenoma - drug therapy</subject><subject>Adenoma - metabolism</subject><subject>Adenoma - pathology</subject><subject>Apoptosis - drug effects</subject><subject>Biological and medical sciences</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation - drug effects</subject><subject>Chemotherapy, Adjuvant</subject><subject>Cyclin D1 - genetics</subject><subject>Cyclin D1 - metabolism</subject><subject>DNA-Binding Proteins - genetics</subject><subject>DNA-Binding Proteins - metabolism</subject><subject>Dose-Response Relationship, Drug</subject><subject>Down-Regulation - drug effects</subject><subject>Endocrinopathies</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Humans</subject><subject>Lithium Compounds - pharmacology</subject><subject>Lithium Compounds - therapeutic use</subject><subject>Malignant tumors</subject><subject>Medical sciences</subject><subject>Non tumoral diseases. Target tissue resistance. Benign neoplasms</subject><subject>Nuclear Receptor Subfamily 4, Group A, Member 1</subject><subject>Proto-Oncogene Proteins c-fos - genetics</subject><subject>Proto-Oncogene Proteins c-fos - metabolism</subject><subject>Receptors, Steroid - genetics</subject><subject>Receptors, Steroid - metabolism</subject><subject>Signal Transduction - drug effects</subject><subject>Thyroid Neoplasms - drug therapy</subject><subject>Thyroid Neoplasms - metabolism</subject><subject>Thyroid Neoplasms - pathology</subject><subject>Thyroid. Thyroid axis (diseases)</subject><subject>Vertebrates: endocrinology</subject><subject>Wnt Proteins - genetics</subject><subject>Wnt Proteins - metabolism</subject><issn>0300-0664</issn><issn>1365-2265</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkF1r2zAUhsVYWdOsf2HoZpd29WFb9sUGJe2aQclgdKz0RsjyUaLMtorkLMm_n9yEdLubbo7gPO85hwchTElK47tap5QXecJYkaeMkDIlnGdVunuDJqfGWzQhnJCEFEV2ji5CWBNC8pKId-icloIJQcoJUjdu2ycelptWDdb12Bm8-J5dU2x7bFzbWh07Hg-rvXe2wVp5bXvXqYBtwB7C4Dw0L6Tb2n6JWzus7KbDgwc1dNAP79GZUW2Ay2Odoh9fbh9m8-T-293X2fV9ovOMVEkOospYUzWqLAG0yCDXUHPIG12ZmlemaGqoGQcDlTKaxMKJ0gwKxRsoDZ-iz4e5z5u6g0bH1V618tnbTvm9dMrKfzu9Xcml-y2ZyBiPAqeoPAzQ3oXgwZyylMhRu1zL0a4c7cpRu3zRLncx-uHv3a_Bo-cIfDwCKmjVGq96bcOJY5TyihVF5D4duK1tYf_fB8jZ7WL8xXxyyNswwO6UV_6XLAQXufy5uJPzm4f54xPl8on_AdIkshY</recordid><startdate>200903</startdate><enddate>200903</enddate><creator>Camacho, Cléber P.</creator><creator>Latini, Flavia R. M.</creator><creator>Oler, Gisele</creator><creator>Hojaij, Flavio C.</creator><creator>Maciel, Rui M. B.</creator><creator>Riggins, Gregory J.</creator><creator>Cerutti, Janete M.</creator><general>Blackwell Publishing Ltd</general><general>Blackwell</general><scope>BSCLL</scope><scope>IQODW</scope><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>200903</creationdate><title>Down-regulation of NR4A1 in follicular thyroid carcinomas is restored following lithium treatment</title><author>Camacho, Cléber P. ; Latini, Flavia R. M. ; Oler, Gisele ; Hojaij, Flavio C. ; Maciel, Rui M. B. ; Riggins, Gregory J. ; Cerutti, Janete M.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5409-5e7942d9da88eec74e5ceb3e5dc9fb39f6dbeb23efe9afc0fe930ac2e6a3de8f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Adenocarcinoma, Follicular - drug therapy</topic><topic>Adenocarcinoma, Follicular - metabolism</topic><topic>Adenocarcinoma, Follicular - pathology</topic><topic>Adenoma - drug therapy</topic><topic>Adenoma - metabolism</topic><topic>Adenoma - pathology</topic><topic>Apoptosis - drug effects</topic><topic>Biological and medical sciences</topic><topic>Cell Line, Tumor</topic><topic>Cell Proliferation - drug effects</topic><topic>Chemotherapy, Adjuvant</topic><topic>Cyclin D1 - genetics</topic><topic>Cyclin D1 - metabolism</topic><topic>DNA-Binding Proteins - genetics</topic><topic>DNA-Binding Proteins - metabolism</topic><topic>Dose-Response Relationship, Drug</topic><topic>Down-Regulation - drug effects</topic><topic>Endocrinopathies</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Humans</topic><topic>Lithium Compounds - pharmacology</topic><topic>Lithium Compounds - therapeutic use</topic><topic>Malignant tumors</topic><topic>Medical sciences</topic><topic>Non tumoral diseases. Target tissue resistance. Benign neoplasms</topic><topic>Nuclear Receptor Subfamily 4, Group A, Member 1</topic><topic>Proto-Oncogene Proteins c-fos - genetics</topic><topic>Proto-Oncogene Proteins c-fos - metabolism</topic><topic>Receptors, Steroid - genetics</topic><topic>Receptors, Steroid - metabolism</topic><topic>Signal Transduction - drug effects</topic><topic>Thyroid Neoplasms - drug therapy</topic><topic>Thyroid Neoplasms - metabolism</topic><topic>Thyroid Neoplasms - pathology</topic><topic>Thyroid. Thyroid axis (diseases)</topic><topic>Vertebrates: endocrinology</topic><topic>Wnt Proteins - genetics</topic><topic>Wnt Proteins - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Camacho, Cléber P.</creatorcontrib><creatorcontrib>Latini, Flavia R. M.</creatorcontrib><creatorcontrib>Oler, Gisele</creatorcontrib><creatorcontrib>Hojaij, Flavio C.</creatorcontrib><creatorcontrib>Maciel, Rui M. B.</creatorcontrib><creatorcontrib>Riggins, Gregory J.</creatorcontrib><creatorcontrib>Cerutti, Janete M.</creatorcontrib><collection>Istex</collection><collection>Pascal-Francis</collection><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>Clinical endocrinology (Oxford)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Camacho, Cléber P.</au><au>Latini, Flavia R. M.</au><au>Oler, Gisele</au><au>Hojaij, Flavio C.</au><au>Maciel, Rui M. B.</au><au>Riggins, Gregory J.</au><au>Cerutti, Janete M.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Down-regulation of NR4A1 in follicular thyroid carcinomas is restored following lithium treatment</atitle><jtitle>Clinical endocrinology (Oxford)</jtitle><addtitle>Clin Endocrinol (Oxf)</addtitle><date>2009-03</date><risdate>2009</risdate><volume>70</volume><issue>3</issue><spage>475</spage><epage>483</epage><pages>475-483</pages><issn>0300-0664</issn><eissn>1365-2265</eissn><coden>CLECAP</coden><abstract>Summary
Introduction The identification of follicular thyroid adenoma‐associated transcripts will lead to a better understanding of the events involved in pathogenesis and progression of follicular tumours. Using Serial Analysis of Gene Expression, we identified five genes that are absent in a malignant follicular thyroid carcinoma (FTC) library, but expressed in follicular adenoma (FTA) and normal thyroid libraries.
Methods NR4A1, one of the five genes, was validated in a set of 27 normal thyroid tissues, 10 FTAs and 14 FTCs and three thyroid carcinoma cell lines by real time PCR. NR4A1 can be transiently increased by a variety of stimuli, including lithium, which is used as adjuvant therapy of thyroid carcinoma with 131I. We tested if lithium could restore NR4A1 expression. The expression of other genes potentially involved in the same signalling pathway was tested. To this end, lithium was used at different concentration (10 mm or 20 mm) and time (2 h and 24 h) and the level of expression was tested by quantitative PCR. We next tested if Lithium could affect cell growth and apoptosis.
Results We observed that NR4A1 expression was under‐expressed in most of the FTCs investigated, compared with expression in normal thyroid tissues and FTAs. We also found a positive correlation between NR4A1 and FOSB gene expression. Lithium induced NR4A1 and FOSB expression, reduced CCDN1 expression, inhibited cell growth and triggered apoptosis in a FTC cell line.
Conclusions NR4A1 is under‐expressed in most of FTCs. The loss of expression of both NR4A1 and the Wnt pathway gene FOSB was correlated with malignancy. This is consistent with the hypothesis that its loss of expression is part of the transformation process of FTCs, either as a direct or indirect consequence of Wnt pathway alterations. Lithium restores NR4A1 expression, induces apoptosis and reduces cell growth. These findings may explain a possible molecular mechanism of lithium's therapeutic action.</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>18727708</pmid><doi>10.1111/j.1365-2265.2008.03349.x</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adenocarcinoma, Follicular - drug therapy Adenocarcinoma, Follicular - metabolism Adenocarcinoma, Follicular - pathology Adenoma - drug therapy Adenoma - metabolism Adenoma - pathology Apoptosis - drug effects Biological and medical sciences Cell Line, Tumor Cell Proliferation - drug effects Chemotherapy, Adjuvant Cyclin D1 - genetics Cyclin D1 - metabolism DNA-Binding Proteins - genetics DNA-Binding Proteins - metabolism Dose-Response Relationship, Drug Down-Regulation - drug effects Endocrinopathies Fundamental and applied biological sciences. Psychology Humans Lithium Compounds - pharmacology Lithium Compounds - therapeutic use Malignant tumors Medical sciences Non tumoral diseases. Target tissue resistance. Benign neoplasms Nuclear Receptor Subfamily 4, Group A, Member 1 Proto-Oncogene Proteins c-fos - genetics Proto-Oncogene Proteins c-fos - metabolism Receptors, Steroid - genetics Receptors, Steroid - metabolism Signal Transduction - drug effects Thyroid Neoplasms - drug therapy Thyroid Neoplasms - metabolism Thyroid Neoplasms - pathology Thyroid. Thyroid axis (diseases) Vertebrates: endocrinology Wnt Proteins - genetics Wnt Proteins - metabolism |
| title | Down-regulation of NR4A1 in follicular thyroid carcinomas is restored following lithium treatment |
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