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Expression of estrogen and progesterone receptors and estrogen metabolizing enzymes in different breast cancer cell lines
Prolonged exposure to estrogens is a significant risk factor for the development of breast cancer. Estrogens exert carcinogenic effects by stimulating cell proliferation or through oxidative metabolism that forms DNA-damaging species. In the present study, we aimed to provide a better understanding...
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| Published in: | Chemico-biological interactions 2011-05, Vol.191 (1), p.206-216 |
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| container_title | Chemico-biological interactions |
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| creator | Hevir, N. Trošt, N. Debeljak, N. Lanišnik Rižner, T. |
| description | Prolonged exposure to estrogens is a significant risk factor for the development of breast cancer. Estrogens exert carcinogenic effects by stimulating cell proliferation or through oxidative metabolism that forms DNA-damaging species. In the present study, we aimed to provide a better understanding of estrogen metabolism and actions in breast cancer, and to characterize model breast cancer cell lines. We determined the expression profiles of the genes for the estrogen and progesterone receptors, and for 18 estrogen-metabolizing enzymes in eight cell lines: MCF-7, MCF-10A, T47D, SKBR3, MDA-MB-231, MDA-MB-361, Hs-578T and Hs-578Bst cells. Similar gene expression profiles of these receptors and enzymes for the formation of estradiol via the aromatase and sulfatase pathways were observed in the MCF-7 and T47D metastatic cell lines. The MDA-MB-361 cells expressed
ESR1,
ESR2 and
PGR as well, but differed in expression of the estrogen-metabolizing enzymes. In the MDA-MB-231 and SKBR3 cells, all of these estrogen-forming enzymes were expressed, although the lack of
ESR1 and the low levels of
ESR2 expression suggested that the estrogens can only act via non-ER mediated pathways. In the non-tumorigenic MCF-10A cell line, the key enzymes of the aromatase pathway were not expressed, and the sulfatase pathway also had a marginal role. The comparison between gene expression profiles of the non-tumorigenic Hs-578Bst cells and the cancerous Hs-578T cells revealed that they can both form estrogens via the sulfatase pathway, while the aromatase pathway is less important in the Hs-578Bst cells. The Hs-578T cells showed low levels of
ESR1,
ESR2 and
PGR expression, while only
ESR1 and
ESR2 expression was detected in the Hs-578Bst cells. Our data show that the cell lines examined provide the full range of model systems and should further be compared with the expression profiles of breast cancer specimens. |
| doi_str_mv | 10.1016/j.cbi.2010.12.013 |
| format | article |
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ESR1,
ESR2 and
PGR as well, but differed in expression of the estrogen-metabolizing enzymes. In the MDA-MB-231 and SKBR3 cells, all of these estrogen-forming enzymes were expressed, although the lack of
ESR1 and the low levels of
ESR2 expression suggested that the estrogens can only act via non-ER mediated pathways. In the non-tumorigenic MCF-10A cell line, the key enzymes of the aromatase pathway were not expressed, and the sulfatase pathway also had a marginal role. The comparison between gene expression profiles of the non-tumorigenic Hs-578Bst cells and the cancerous Hs-578T cells revealed that they can both form estrogens via the sulfatase pathway, while the aromatase pathway is less important in the Hs-578Bst cells. The Hs-578T cells showed low levels of
ESR1,
ESR2 and
PGR expression, while only
ESR1 and
ESR2 expression was detected in the Hs-578Bst cells. Our data show that the cell lines examined provide the full range of model systems and should further be compared with the expression profiles of breast cancer specimens.</description><identifier>ISSN: 0009-2797</identifier><identifier>EISSN: 1872-7786</identifier><identifier>DOI: 10.1016/j.cbi.2010.12.013</identifier><identifier>PMID: 21182832</identifier><language>eng</language><publisher>Ireland: Elsevier Ireland Ltd</publisher><subject>17β-Hydroxysteroid dehydrogenases (17β-HSDs) ; aerobiosis ; Aldo-keto reductases (AKRs) ; Aromatase ; arylsulfatase ; breast neoplasms ; Breast Neoplasms - enzymology ; Breast Neoplasms - genetics ; Breast Neoplasms - metabolism ; Breast Neoplasms - pathology ; carcinogenicity ; Catechol-O-methyl transferase (COMT) ; Cell Line, Tumor ; cell proliferation ; Enzymes - genetics ; Enzymes - metabolism ; estradiol ; estrogen receptors ; Estrogens - biosynthesis ; Estrogens - metabolism ; gene expression ; Gene Expression Regulation, Neoplastic ; genes ; Humans ; metastasis ; plant growth substances ; progesterone receptors ; Receptors, Estrogen - genetics ; Receptors, Progesterone - genetics ; risk factors ; Sulfatase ; Sulfotransferases ; UDP Glucuronosyl transferase (UGT) ; unspecific monooxygenase</subject><ispartof>Chemico-biological interactions, 2011-05, Vol.191 (1), p.206-216</ispartof><rights>2010 Elsevier Ireland Ltd</rights><rights>Copyright © 2010 Elsevier Ireland Ltd. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c409t-93fd42f44ebd193a42aa71ccf6b98ec41113ad1aa7176a5f8978618ce7ce29f53</citedby><cites>FETCH-LOGICAL-c409t-93fd42f44ebd193a42aa71ccf6b98ec41113ad1aa7176a5f8978618ce7ce29f53</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,786,790,27957,27958</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21182832$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hevir, N.</creatorcontrib><creatorcontrib>Trošt, N.</creatorcontrib><creatorcontrib>Debeljak, N.</creatorcontrib><creatorcontrib>Lanišnik Rižner, T.</creatorcontrib><title>Expression of estrogen and progesterone receptors and estrogen metabolizing enzymes in different breast cancer cell lines</title><title>Chemico-biological interactions</title><addtitle>Chem Biol Interact</addtitle><description>Prolonged exposure to estrogens is a significant risk factor for the development of breast cancer. Estrogens exert carcinogenic effects by stimulating cell proliferation or through oxidative metabolism that forms DNA-damaging species. In the present study, we aimed to provide a better understanding of estrogen metabolism and actions in breast cancer, and to characterize model breast cancer cell lines. We determined the expression profiles of the genes for the estrogen and progesterone receptors, and for 18 estrogen-metabolizing enzymes in eight cell lines: MCF-7, MCF-10A, T47D, SKBR3, MDA-MB-231, MDA-MB-361, Hs-578T and Hs-578Bst cells. Similar gene expression profiles of these receptors and enzymes for the formation of estradiol via the aromatase and sulfatase pathways were observed in the MCF-7 and T47D metastatic cell lines. The MDA-MB-361 cells expressed
ESR1,
ESR2 and
PGR as well, but differed in expression of the estrogen-metabolizing enzymes. In the MDA-MB-231 and SKBR3 cells, all of these estrogen-forming enzymes were expressed, although the lack of
ESR1 and the low levels of
ESR2 expression suggested that the estrogens can only act via non-ER mediated pathways. In the non-tumorigenic MCF-10A cell line, the key enzymes of the aromatase pathway were not expressed, and the sulfatase pathway also had a marginal role. The comparison between gene expression profiles of the non-tumorigenic Hs-578Bst cells and the cancerous Hs-578T cells revealed that they can both form estrogens via the sulfatase pathway, while the aromatase pathway is less important in the Hs-578Bst cells. The Hs-578T cells showed low levels of
ESR1,
ESR2 and
PGR expression, while only
ESR1 and
ESR2 expression was detected in the Hs-578Bst cells. Our data show that the cell lines examined provide the full range of model systems and should further be compared with the expression profiles of breast cancer specimens.</description><subject>17β-Hydroxysteroid dehydrogenases (17β-HSDs)</subject><subject>aerobiosis</subject><subject>Aldo-keto reductases (AKRs)</subject><subject>Aromatase</subject><subject>arylsulfatase</subject><subject>breast neoplasms</subject><subject>Breast Neoplasms - enzymology</subject><subject>Breast Neoplasms - genetics</subject><subject>Breast Neoplasms - metabolism</subject><subject>Breast Neoplasms - pathology</subject><subject>carcinogenicity</subject><subject>Catechol-O-methyl transferase (COMT)</subject><subject>Cell Line, Tumor</subject><subject>cell proliferation</subject><subject>Enzymes - genetics</subject><subject>Enzymes - metabolism</subject><subject>estradiol</subject><subject>estrogen receptors</subject><subject>Estrogens - biosynthesis</subject><subject>Estrogens - metabolism</subject><subject>gene expression</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>genes</subject><subject>Humans</subject><subject>metastasis</subject><subject>plant growth substances</subject><subject>progesterone receptors</subject><subject>Receptors, Estrogen - genetics</subject><subject>Receptors, Progesterone - genetics</subject><subject>risk factors</subject><subject>Sulfatase</subject><subject>Sulfotransferases</subject><subject>UDP Glucuronosyl transferase (UGT)</subject><subject>unspecific monooxygenase</subject><issn>0009-2797</issn><issn>1872-7786</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><recordid>eNp9kU1v1DAQQC0EokvLD-ACPvaSxeNk_SFOqGoLUiUOtGfLccYrrxJ7sbOI7a_H6ZYeOdkzfjOaeSbkA7A1MBCfd2vXhzVnS8zXDNpXZAVK8kZKJV6TFWNMN1xqeUbelbKrIeMde0vOOIDiquUrcrz-s89YSkiRJk-xzDltMVIbB7pfrmXGnCLSjA73c8rl6emFm3C2fRrDY4hbivHxOGGhIdIheI8Z40z7jLbM1NnoMFOH40jHELFckDfejgXfP5_n5OHm-v7qW3P34_b71de7xnVMz41u_dBx33XYD6Bb23FrJTjnRa8Vug4AWjvAkpTCbrzSdXdQDqVDrv2mPSeXp751nV-HOriZQlnGsBHToRgQSgohpF5QOKEup1IyerPPYbL5aICZxbjZmWrcLMYNcFON15qPz-0P_YTDS8U_xRX4dAK8TcZucyjm4WftsKm_IVS7gUp8ORFYNfwOmE1xAauuIVTrsxlS-M8AfwFrEZ0V</recordid><startdate>20110530</startdate><enddate>20110530</enddate><creator>Hevir, N.</creator><creator>Trošt, N.</creator><creator>Debeljak, N.</creator><creator>Lanišnik Rižner, T.</creator><general>Elsevier Ireland Ltd</general><scope>FBQ</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>7U7</scope><scope>C1K</scope></search><sort><creationdate>20110530</creationdate><title>Expression of estrogen and progesterone receptors and estrogen metabolizing enzymes in different breast cancer cell lines</title><author>Hevir, N. ; Trošt, N. ; Debeljak, N. ; Lanišnik Rižner, T.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c409t-93fd42f44ebd193a42aa71ccf6b98ec41113ad1aa7176a5f8978618ce7ce29f53</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>17β-Hydroxysteroid dehydrogenases (17β-HSDs)</topic><topic>aerobiosis</topic><topic>Aldo-keto reductases (AKRs)</topic><topic>Aromatase</topic><topic>arylsulfatase</topic><topic>breast neoplasms</topic><topic>Breast Neoplasms - enzymology</topic><topic>Breast Neoplasms - genetics</topic><topic>Breast Neoplasms - metabolism</topic><topic>Breast Neoplasms - pathology</topic><topic>carcinogenicity</topic><topic>Catechol-O-methyl transferase (COMT)</topic><topic>Cell Line, Tumor</topic><topic>cell proliferation</topic><topic>Enzymes - genetics</topic><topic>Enzymes - metabolism</topic><topic>estradiol</topic><topic>estrogen receptors</topic><topic>Estrogens - biosynthesis</topic><topic>Estrogens - metabolism</topic><topic>gene expression</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>genes</topic><topic>Humans</topic><topic>metastasis</topic><topic>plant growth substances</topic><topic>progesterone receptors</topic><topic>Receptors, Estrogen - genetics</topic><topic>Receptors, Progesterone - genetics</topic><topic>risk factors</topic><topic>Sulfatase</topic><topic>Sulfotransferases</topic><topic>UDP Glucuronosyl transferase (UGT)</topic><topic>unspecific monooxygenase</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hevir, N.</creatorcontrib><creatorcontrib>Trošt, N.</creatorcontrib><creatorcontrib>Debeljak, N.</creatorcontrib><creatorcontrib>Lanišnik Rižner, T.</creatorcontrib><collection>AGRIS</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Toxicology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><jtitle>Chemico-biological interactions</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hevir, N.</au><au>Trošt, N.</au><au>Debeljak, N.</au><au>Lanišnik Rižner, T.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Expression of estrogen and progesterone receptors and estrogen metabolizing enzymes in different breast cancer cell lines</atitle><jtitle>Chemico-biological interactions</jtitle><addtitle>Chem Biol Interact</addtitle><date>2011-05-30</date><risdate>2011</risdate><volume>191</volume><issue>1</issue><spage>206</spage><epage>216</epage><pages>206-216</pages><issn>0009-2797</issn><eissn>1872-7786</eissn><notes>http://dx.doi.org/10.1016/j.cbi.2010.12.013</notes><notes>ObjectType-Article-1</notes><notes>SourceType-Scholarly Journals-1</notes><notes>ObjectType-Feature-2</notes><notes>content type line 23</notes><abstract>Prolonged exposure to estrogens is a significant risk factor for the development of breast cancer. Estrogens exert carcinogenic effects by stimulating cell proliferation or through oxidative metabolism that forms DNA-damaging species. In the present study, we aimed to provide a better understanding of estrogen metabolism and actions in breast cancer, and to characterize model breast cancer cell lines. We determined the expression profiles of the genes for the estrogen and progesterone receptors, and for 18 estrogen-metabolizing enzymes in eight cell lines: MCF-7, MCF-10A, T47D, SKBR3, MDA-MB-231, MDA-MB-361, Hs-578T and Hs-578Bst cells. Similar gene expression profiles of these receptors and enzymes for the formation of estradiol via the aromatase and sulfatase pathways were observed in the MCF-7 and T47D metastatic cell lines. The MDA-MB-361 cells expressed
ESR1,
ESR2 and
PGR as well, but differed in expression of the estrogen-metabolizing enzymes. In the MDA-MB-231 and SKBR3 cells, all of these estrogen-forming enzymes were expressed, although the lack of
ESR1 and the low levels of
ESR2 expression suggested that the estrogens can only act via non-ER mediated pathways. In the non-tumorigenic MCF-10A cell line, the key enzymes of the aromatase pathway were not expressed, and the sulfatase pathway also had a marginal role. The comparison between gene expression profiles of the non-tumorigenic Hs-578Bst cells and the cancerous Hs-578T cells revealed that they can both form estrogens via the sulfatase pathway, while the aromatase pathway is less important in the Hs-578Bst cells. The Hs-578T cells showed low levels of
ESR1,
ESR2 and
PGR expression, while only
ESR1 and
ESR2 expression was detected in the Hs-578Bst cells. Our data show that the cell lines examined provide the full range of model systems and should further be compared with the expression profiles of breast cancer specimens.</abstract><cop>Ireland</cop><pub>Elsevier Ireland Ltd</pub><pmid>21182832</pmid><doi>10.1016/j.cbi.2010.12.013</doi><tpages>11</tpages></addata></record> |
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| ispartof | Chemico-biological interactions, 2011-05, Vol.191 (1), p.206-216 |
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| source | ScienceDirect Freedom Collection 2022-2024 |
| subjects | 17β-Hydroxysteroid dehydrogenases (17β-HSDs) aerobiosis Aldo-keto reductases (AKRs) Aromatase arylsulfatase breast neoplasms Breast Neoplasms - enzymology Breast Neoplasms - genetics Breast Neoplasms - metabolism Breast Neoplasms - pathology carcinogenicity Catechol-O-methyl transferase (COMT) Cell Line, Tumor cell proliferation Enzymes - genetics Enzymes - metabolism estradiol estrogen receptors Estrogens - biosynthesis Estrogens - metabolism gene expression Gene Expression Regulation, Neoplastic genes Humans metastasis plant growth substances progesterone receptors Receptors, Estrogen - genetics Receptors, Progesterone - genetics risk factors Sulfatase Sulfotransferases UDP Glucuronosyl transferase (UGT) unspecific monooxygenase |
| title | Expression of estrogen and progesterone receptors and estrogen metabolizing enzymes in different breast cancer cell lines |
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