Androgen receptor activation decreases proliferation in thyroid cancer cells
The American Cancer Society predicted more than 52 000 new cases of thyroid cancer in 2020, making it the most prevalent endocrine malignancy. Due to the approximately threefold higher incidence of thyroid cancer in women, we hypothesize that androgens and/or androgen receptors play a protective rol...
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| Veröffentlicht in: | Journal of cellular biochemistry 2021-09, Vol.122 (9), p.1113-1125 |
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| creator | Jones, Melanie E. O'Connell, Timmy J. Zhao, Hong Darzynkiewicz, Zgibniew Gupta, Anvita Buchsbaum, Joseph Shin, Edward Iacob, Codrin Suslina, Nina Moscatello, Augustine Schantz, Stimson Tiwari, Raj Geliebter, Jan |
| description | The American Cancer Society predicted more than 52 000 new cases of thyroid cancer in 2020, making it the most prevalent endocrine malignancy. Due to the approximately threefold higher incidence of thyroid cancer in women, we hypothesize that androgens and/or androgen receptors play a protective role and that thyroid cancer in men represents an escape from androgen‐mediated cell regulation. The analysis of androgen receptor (AR) expression in patient tissue samples identified a 2.7‐fold reduction in AR expression (p |
| doi_str_mv | 10.1002/jcb.29934 |
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Due to the approximately threefold higher incidence of thyroid cancer in women, we hypothesize that androgens and/or androgen receptors play a protective role and that thyroid cancer in men represents an escape from androgen‐mediated cell regulation. The analysis of androgen receptor (AR) expression in patient tissue samples identified a 2.7‐fold reduction in AR expression (p < 0.005) in papillary thyroid cancer compared with matched, normal tissue. An in vitro cell model was developed by stably transfecting AR into 8505C undifferentiated thyroid cancer cells (resulting in clone 84E7). The addition of DHT to the clone 84E7 resulted in AR translocation into the nucleus and a 70% reduction in proliferation, with a shift in the cell cycle toward G1 arrest. RNASeq analysis revealed significant changes in mRNA levels associated with proliferation, cell cycle, and cell cycle regulation. Furthermore, androgen significantly decreased the levels of the G1‐associated cell cycle progression proteins cdc25a CDK6 CDK4 and CDK2 as well as increased the levels of the cell cycle inhibitors, p27 and p21. The data strongly suggest that DHT induces a G1 arrest in androgen‐responsive thyroid cancer cells. Together, these data support our hypothesis that AR/androgen may play a protective, antiproliferative role and are consistent with younger men having a lower incidence of thyroid cancer than women.</description><identifier>ISSN: 0730-2312</identifier><identifier>EISSN: 1097-4644</identifier><identifier>DOI: 10.1002/jcb.29934</identifier><identifier>PMID: 33876852</identifier><language>eng</language><publisher>United States: Wiley Subscription Services, Inc</publisher><subject>androgen ; androgen receptor ; Androgen receptors ; Androgens ; Cancer ; Cell cycle ; cell cycle checkpoint ; Cell proliferation ; Cyclin-dependent kinase 2 ; Cyclin-dependent kinase 4 ; Malignancy ; mRNA ; Neuroendocrine tumors ; Papillary thyroid cancer ; Receptor mechanisms ; Receptors ; Reduction ; Thyroid ; Thyroid cancer ; Translocation</subject><ispartof>Journal of cellular biochemistry, 2021-09, Vol.122 (9), p.1113-1125</ispartof><rights>2021 Wiley Periodicals LLC</rights><rights>2021 Wiley Periodicals LLC.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3534-fefb2d6a27cb95d4a3cf9cbd501da2d519792cdcb1cf867626cb42b5865c253c3</citedby><cites>FETCH-LOGICAL-c3534-fefb2d6a27cb95d4a3cf9cbd501da2d519792cdcb1cf867626cb42b5865c253c3</cites><orcidid>0000-0002-6768-6866</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fjcb.29934$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fjcb.29934$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33876852$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Jones, Melanie E.</creatorcontrib><creatorcontrib>O'Connell, Timmy J.</creatorcontrib><creatorcontrib>Zhao, Hong</creatorcontrib><creatorcontrib>Darzynkiewicz, Zgibniew</creatorcontrib><creatorcontrib>Gupta, Anvita</creatorcontrib><creatorcontrib>Buchsbaum, Joseph</creatorcontrib><creatorcontrib>Shin, Edward</creatorcontrib><creatorcontrib>Iacob, Codrin</creatorcontrib><creatorcontrib>Suslina, Nina</creatorcontrib><creatorcontrib>Moscatello, Augustine</creatorcontrib><creatorcontrib>Schantz, Stimson</creatorcontrib><creatorcontrib>Tiwari, Raj</creatorcontrib><creatorcontrib>Geliebter, Jan</creatorcontrib><title>Androgen receptor activation decreases proliferation in thyroid cancer cells</title><title>Journal of cellular biochemistry</title><addtitle>J Cell Biochem</addtitle><description>The American Cancer Society predicted more than 52 000 new cases of thyroid cancer in 2020, making it the most prevalent endocrine malignancy. Due to the approximately threefold higher incidence of thyroid cancer in women, we hypothesize that androgens and/or androgen receptors play a protective role and that thyroid cancer in men represents an escape from androgen‐mediated cell regulation. The analysis of androgen receptor (AR) expression in patient tissue samples identified a 2.7‐fold reduction in AR expression (p < 0.005) in papillary thyroid cancer compared with matched, normal tissue. An in vitro cell model was developed by stably transfecting AR into 8505C undifferentiated thyroid cancer cells (resulting in clone 84E7). The addition of DHT to the clone 84E7 resulted in AR translocation into the nucleus and a 70% reduction in proliferation, with a shift in the cell cycle toward G1 arrest. RNASeq analysis revealed significant changes in mRNA levels associated with proliferation, cell cycle, and cell cycle regulation. Furthermore, androgen significantly decreased the levels of the G1‐associated cell cycle progression proteins cdc25a CDK6 CDK4 and CDK2 as well as increased the levels of the cell cycle inhibitors, p27 and p21. The data strongly suggest that DHT induces a G1 arrest in androgen‐responsive thyroid cancer cells. Together, these data support our hypothesis that AR/androgen may play a protective, antiproliferative role and are consistent with younger men having a lower incidence of thyroid cancer than women.</description><subject>androgen</subject><subject>androgen receptor</subject><subject>Androgen receptors</subject><subject>Androgens</subject><subject>Cancer</subject><subject>Cell cycle</subject><subject>cell cycle checkpoint</subject><subject>Cell proliferation</subject><subject>Cyclin-dependent kinase 2</subject><subject>Cyclin-dependent kinase 4</subject><subject>Malignancy</subject><subject>mRNA</subject><subject>Neuroendocrine tumors</subject><subject>Papillary thyroid cancer</subject><subject>Receptor mechanisms</subject><subject>Receptors</subject><subject>Reduction</subject><subject>Thyroid</subject><subject>Thyroid cancer</subject><subject>Translocation</subject><issn>0730-2312</issn><issn>1097-4644</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><recordid>eNp10M1LwzAYBvAgipvTg_-AFLzooVvy5qPtUYefDLzouaRvUu3o2pm0yv57Mzs9CJ4C4ZcnDw8hp4xOGaUwW2IxhSzjYo-MGc2SWCgh9smYJpzGwBmMyJH3S0ppQHBIRpyniUoljMniqjGufbVN5Czadde6SGNXfeiuapvIWHRWe-ujtWvrqrRuuK-aqHvbuLYyEeoGrYvQ1rU_Jgelrr092Z0T8nJ78zy_jxdPdw_zq0WMXHIRl7YswCgNCRaZNEJzLDMsjKTMaDCSZUkGaLBgWKYqUaCwEFDIVEkEyZFPyMWQG1q999Z3-ary2wa6sW3vc5BMqvAy_DYh53_osu1dE9oFpQBApEwFdTkodK33zpb52lUr7TY5o_l24jxMnH9PHOzZLrEvVtb8yp9NA5gN4LOq7eb_pPxxfj1EfgEIJIWx</recordid><startdate>202109</startdate><enddate>202109</enddate><creator>Jones, Melanie E.</creator><creator>O'Connell, Timmy J.</creator><creator>Zhao, Hong</creator><creator>Darzynkiewicz, Zgibniew</creator><creator>Gupta, Anvita</creator><creator>Buchsbaum, Joseph</creator><creator>Shin, Edward</creator><creator>Iacob, Codrin</creator><creator>Suslina, Nina</creator><creator>Moscatello, Augustine</creator><creator>Schantz, Stimson</creator><creator>Tiwari, Raj</creator><creator>Geliebter, Jan</creator><general>Wiley Subscription Services, Inc</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QL</scope><scope>7QP</scope><scope>7QR</scope><scope>7T7</scope><scope>7TK</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>M7N</scope><scope>P64</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-6768-6866</orcidid></search><sort><creationdate>202109</creationdate><title>Androgen receptor activation decreases proliferation in thyroid cancer cells</title><author>Jones, Melanie E. ; O'Connell, Timmy J. ; Zhao, Hong ; Darzynkiewicz, Zgibniew ; Gupta, Anvita ; Buchsbaum, Joseph ; Shin, Edward ; Iacob, Codrin ; Suslina, Nina ; Moscatello, Augustine ; Schantz, Stimson ; Tiwari, Raj ; Geliebter, Jan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3534-fefb2d6a27cb95d4a3cf9cbd501da2d519792cdcb1cf867626cb42b5865c253c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>androgen</topic><topic>androgen receptor</topic><topic>Androgen receptors</topic><topic>Androgens</topic><topic>Cancer</topic><topic>Cell cycle</topic><topic>cell cycle checkpoint</topic><topic>Cell proliferation</topic><topic>Cyclin-dependent kinase 2</topic><topic>Cyclin-dependent kinase 4</topic><topic>Malignancy</topic><topic>mRNA</topic><topic>Neuroendocrine tumors</topic><topic>Papillary thyroid cancer</topic><topic>Receptor mechanisms</topic><topic>Receptors</topic><topic>Reduction</topic><topic>Thyroid</topic><topic>Thyroid cancer</topic><topic>Translocation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Jones, Melanie E.</creatorcontrib><creatorcontrib>O'Connell, Timmy J.</creatorcontrib><creatorcontrib>Zhao, Hong</creatorcontrib><creatorcontrib>Darzynkiewicz, Zgibniew</creatorcontrib><creatorcontrib>Gupta, Anvita</creatorcontrib><creatorcontrib>Buchsbaum, Joseph</creatorcontrib><creatorcontrib>Shin, Edward</creatorcontrib><creatorcontrib>Iacob, Codrin</creatorcontrib><creatorcontrib>Suslina, Nina</creatorcontrib><creatorcontrib>Moscatello, Augustine</creatorcontrib><creatorcontrib>Schantz, Stimson</creatorcontrib><creatorcontrib>Tiwari, Raj</creatorcontrib><creatorcontrib>Geliebter, Jan</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Neurosciences Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of cellular biochemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Jones, Melanie E.</au><au>O'Connell, Timmy J.</au><au>Zhao, Hong</au><au>Darzynkiewicz, Zgibniew</au><au>Gupta, Anvita</au><au>Buchsbaum, Joseph</au><au>Shin, Edward</au><au>Iacob, Codrin</au><au>Suslina, Nina</au><au>Moscatello, Augustine</au><au>Schantz, Stimson</au><au>Tiwari, Raj</au><au>Geliebter, Jan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Androgen receptor activation decreases proliferation in thyroid cancer cells</atitle><jtitle>Journal of cellular biochemistry</jtitle><addtitle>J Cell Biochem</addtitle><date>2021-09</date><risdate>2021</risdate><volume>122</volume><issue>9</issue><spage>1113</spage><epage>1125</epage><pages>1113-1125</pages><issn>0730-2312</issn><eissn>1097-4644</eissn><abstract>The American Cancer Society predicted more than 52 000 new cases of thyroid cancer in 2020, making it the most prevalent endocrine malignancy. Due to the approximately threefold higher incidence of thyroid cancer in women, we hypothesize that androgens and/or androgen receptors play a protective role and that thyroid cancer in men represents an escape from androgen‐mediated cell regulation. The analysis of androgen receptor (AR) expression in patient tissue samples identified a 2.7‐fold reduction in AR expression (p < 0.005) in papillary thyroid cancer compared with matched, normal tissue. An in vitro cell model was developed by stably transfecting AR into 8505C undifferentiated thyroid cancer cells (resulting in clone 84E7). The addition of DHT to the clone 84E7 resulted in AR translocation into the nucleus and a 70% reduction in proliferation, with a shift in the cell cycle toward G1 arrest. RNASeq analysis revealed significant changes in mRNA levels associated with proliferation, cell cycle, and cell cycle regulation. Furthermore, androgen significantly decreased the levels of the G1‐associated cell cycle progression proteins cdc25a CDK6 CDK4 and CDK2 as well as increased the levels of the cell cycle inhibitors, p27 and p21. The data strongly suggest that DHT induces a G1 arrest in androgen‐responsive thyroid cancer cells. Together, these data support our hypothesis that AR/androgen may play a protective, antiproliferative role and are consistent with younger men having a lower incidence of thyroid cancer than women.</abstract><cop>United States</cop><pub>Wiley Subscription Services, Inc</pub><pmid>33876852</pmid><doi>10.1002/jcb.29934</doi><tpages>13</tpages><orcidid>https://orcid.org/0000-0002-6768-6866</orcidid></addata></record> |
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| subjects | androgen androgen receptor Androgen receptors Androgens Cancer Cell cycle cell cycle checkpoint Cell proliferation Cyclin-dependent kinase 2 Cyclin-dependent kinase 4 Malignancy mRNA Neuroendocrine tumors Papillary thyroid cancer Receptor mechanisms Receptors Reduction Thyroid Thyroid cancer Translocation |
| title | Androgen receptor activation decreases proliferation in thyroid cancer cells |
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