Partial agonist, but not pure antiestrogens stimulate doming, a marker of normal differentiation, in the MCF-7 breast cancer cell line
Background: The mechanisms by which tamoxifen inhibits breast tumor growth are not completely understood. Partial agonist antiestrogens such as tamoxifen may cause the estrogen receptor (ER) to interact with genes different from those activated by ER bound to estradiol. Doming is a property often as...
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E-Artikel |
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| Erschienen: |
De Gruyter ; 2012 |
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5 |
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| Reproduktion: |
Walter de Gruyter Online Zeitschriften |
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| Übergeordnetes Werk: |
Enthalten in: Hormone molecular biology and clinical investigation - Berlin : de Gruyter, 2010, 12(2012), 3 vom: 05. Dez., Seite 419-423 |
| Übergeordnetes Werk: |
volume:12 ; year:2012 ; number:3 ; day:05 ; month:12 ; pages:419-423 ; extent:5 |
| Links: |
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| DOI / URN: |
10.1515/hmbci-2012-0034 |
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NLEJ246929286 |
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| 520 | |a Background: The mechanisms by which tamoxifen inhibits breast tumor growth are not completely understood. Partial agonist antiestrogens such as tamoxifen may cause the estrogen receptor (ER) to interact with genes different from those activated by ER bound to estradiol. Doming is a property often associated with, and considered a marker of, differentiation in mammary epithelial cells in culture. This study compared the ability of pure and partial agonist antiestrogens to stimulate doming. Materials and methods: MCF-7 cells grown in medium with 10% calf serum were treated with antiestrogens. Domes were counted in three rows (width of the 4× field) across the flask. Results: Three partial agonist antiestrogens [4-hydroxytamoxifen (OHT), H1285 and RU 39,411] caused dome formation. None of the pure antiestrogens tested (ICI 164,384, ICI 182,780 and RU 58,668) caused doming. Doming was stimulated in a dose-dependent manner starting at 1 nM OHT with maximum stimulation at 10–100 nM. Estradiol did not stimulate doming, but blocked doming at 1%–10% of the OHT concentration. Trichostatin A (TSA) reduced the level of estrogen receptor alpha (ERα) and adding it 24 h before adding OHT prevented dome formation. Conclusions: OHT and the other partial agonist antiestrogens appear to act through the ER to stimulate doming. The ability of tamoxifen to induce a marker of differentiation may play a role in its inhibition of breast tumors. If so, then the fact that other partial agonist antiestrogens share this ability, but that pure antiestrogens lack it, may be an important consideration in developing new antiestrogens for breast cancer therapy. | ||
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10.1515/hmbci-2012-0034 doi artikel_Grundlieferung.pp (DE-627)NLEJ246929286 DE-627 ger DE-627 rakwb Partial agonist, but not pure antiestrogens stimulate doming, a marker of normal differentiation, in the MCF-7 breast cancer cell line De Gruyter 2012 5 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background: The mechanisms by which tamoxifen inhibits breast tumor growth are not completely understood. Partial agonist antiestrogens such as tamoxifen may cause the estrogen receptor (ER) to interact with genes different from those activated by ER bound to estradiol. Doming is a property often associated with, and considered a marker of, differentiation in mammary epithelial cells in culture. This study compared the ability of pure and partial agonist antiestrogens to stimulate doming. Materials and methods: MCF-7 cells grown in medium with 10% calf serum were treated with antiestrogens. Domes were counted in three rows (width of the 4× field) across the flask. Results: Three partial agonist antiestrogens [4-hydroxytamoxifen (OHT), H1285 and RU 39,411] caused dome formation. None of the pure antiestrogens tested (ICI 164,384, ICI 182,780 and RU 58,668) caused doming. Doming was stimulated in a dose-dependent manner starting at 1 nM OHT with maximum stimulation at 10–100 nM. Estradiol did not stimulate doming, but blocked doming at 1%–10% of the OHT concentration. Trichostatin A (TSA) reduced the level of estrogen receptor alpha (ERα) and adding it 24 h before adding OHT prevented dome formation. Conclusions: OHT and the other partial agonist antiestrogens appear to act through the ER to stimulate doming. The ability of tamoxifen to induce a marker of differentiation may play a role in its inhibition of breast tumors. If so, then the fact that other partial agonist antiestrogens share this ability, but that pure antiestrogens lack it, may be an important consideration in developing new antiestrogens for breast cancer therapy. Walter de Gruyter Online Zeitschriften antiestrogens breast cancer differentiation doming MCF-7 Butler, W. Barkley oth D’Amico, Stephen C. oth Glassford, William J. oth Wu, Weizhen oth Enthalten in Hormone molecular biology and clinical investigation Berlin : de Gruyter, 2010 12(2012), 3 vom: 05. Dez., Seite 419-423 (DE-627)NLEJ248235699 (DE-600)2536635-X 1868-1891 nnns volume:12 year:2012 number:3 day:05 month:12 pages:419-423 extent:5 https://doi.org/10.1515/hmbci-2012-0034 Deutschlandweit zugänglich GBV_USEFLAG_U ZDB-1-DGR GBV_NL_ARTICLE AR 12 2012 3 05 12 419-423 5 |
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10.1515/hmbci-2012-0034 doi artikel_Grundlieferung.pp (DE-627)NLEJ246929286 DE-627 ger DE-627 rakwb Partial agonist, but not pure antiestrogens stimulate doming, a marker of normal differentiation, in the MCF-7 breast cancer cell line De Gruyter 2012 5 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background: The mechanisms by which tamoxifen inhibits breast tumor growth are not completely understood. Partial agonist antiestrogens such as tamoxifen may cause the estrogen receptor (ER) to interact with genes different from those activated by ER bound to estradiol. Doming is a property often associated with, and considered a marker of, differentiation in mammary epithelial cells in culture. This study compared the ability of pure and partial agonist antiestrogens to stimulate doming. Materials and methods: MCF-7 cells grown in medium with 10% calf serum were treated with antiestrogens. Domes were counted in three rows (width of the 4× field) across the flask. Results: Three partial agonist antiestrogens [4-hydroxytamoxifen (OHT), H1285 and RU 39,411] caused dome formation. None of the pure antiestrogens tested (ICI 164,384, ICI 182,780 and RU 58,668) caused doming. Doming was stimulated in a dose-dependent manner starting at 1 nM OHT with maximum stimulation at 10–100 nM. Estradiol did not stimulate doming, but blocked doming at 1%–10% of the OHT concentration. Trichostatin A (TSA) reduced the level of estrogen receptor alpha (ERα) and adding it 24 h before adding OHT prevented dome formation. Conclusions: OHT and the other partial agonist antiestrogens appear to act through the ER to stimulate doming. The ability of tamoxifen to induce a marker of differentiation may play a role in its inhibition of breast tumors. If so, then the fact that other partial agonist antiestrogens share this ability, but that pure antiestrogens lack it, may be an important consideration in developing new antiestrogens for breast cancer therapy. Walter de Gruyter Online Zeitschriften antiestrogens breast cancer differentiation doming MCF-7 Butler, W. Barkley oth D’Amico, Stephen C. oth Glassford, William J. oth Wu, Weizhen oth Enthalten in Hormone molecular biology and clinical investigation Berlin : de Gruyter, 2010 12(2012), 3 vom: 05. Dez., Seite 419-423 (DE-627)NLEJ248235699 (DE-600)2536635-X 1868-1891 nnns volume:12 year:2012 number:3 day:05 month:12 pages:419-423 extent:5 https://doi.org/10.1515/hmbci-2012-0034 Deutschlandweit zugänglich GBV_USEFLAG_U ZDB-1-DGR GBV_NL_ARTICLE AR 12 2012 3 05 12 419-423 5 |
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10.1515/hmbci-2012-0034 doi artikel_Grundlieferung.pp (DE-627)NLEJ246929286 DE-627 ger DE-627 rakwb Partial agonist, but not pure antiestrogens stimulate doming, a marker of normal differentiation, in the MCF-7 breast cancer cell line De Gruyter 2012 5 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background: The mechanisms by which tamoxifen inhibits breast tumor growth are not completely understood. Partial agonist antiestrogens such as tamoxifen may cause the estrogen receptor (ER) to interact with genes different from those activated by ER bound to estradiol. Doming is a property often associated with, and considered a marker of, differentiation in mammary epithelial cells in culture. This study compared the ability of pure and partial agonist antiestrogens to stimulate doming. Materials and methods: MCF-7 cells grown in medium with 10% calf serum were treated with antiestrogens. Domes were counted in three rows (width of the 4× field) across the flask. Results: Three partial agonist antiestrogens [4-hydroxytamoxifen (OHT), H1285 and RU 39,411] caused dome formation. None of the pure antiestrogens tested (ICI 164,384, ICI 182,780 and RU 58,668) caused doming. Doming was stimulated in a dose-dependent manner starting at 1 nM OHT with maximum stimulation at 10–100 nM. Estradiol did not stimulate doming, but blocked doming at 1%–10% of the OHT concentration. Trichostatin A (TSA) reduced the level of estrogen receptor alpha (ERα) and adding it 24 h before adding OHT prevented dome formation. Conclusions: OHT and the other partial agonist antiestrogens appear to act through the ER to stimulate doming. The ability of tamoxifen to induce a marker of differentiation may play a role in its inhibition of breast tumors. If so, then the fact that other partial agonist antiestrogens share this ability, but that pure antiestrogens lack it, may be an important consideration in developing new antiestrogens for breast cancer therapy. Walter de Gruyter Online Zeitschriften antiestrogens breast cancer differentiation doming MCF-7 Butler, W. Barkley oth D’Amico, Stephen C. oth Glassford, William J. oth Wu, Weizhen oth Enthalten in Hormone molecular biology and clinical investigation Berlin : de Gruyter, 2010 12(2012), 3 vom: 05. Dez., Seite 419-423 (DE-627)NLEJ248235699 (DE-600)2536635-X 1868-1891 nnns volume:12 year:2012 number:3 day:05 month:12 pages:419-423 extent:5 https://doi.org/10.1515/hmbci-2012-0034 Deutschlandweit zugänglich GBV_USEFLAG_U ZDB-1-DGR GBV_NL_ARTICLE AR 12 2012 3 05 12 419-423 5 |
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10.1515/hmbci-2012-0034 doi artikel_Grundlieferung.pp (DE-627)NLEJ246929286 DE-627 ger DE-627 rakwb Partial agonist, but not pure antiestrogens stimulate doming, a marker of normal differentiation, in the MCF-7 breast cancer cell line De Gruyter 2012 5 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background: The mechanisms by which tamoxifen inhibits breast tumor growth are not completely understood. Partial agonist antiestrogens such as tamoxifen may cause the estrogen receptor (ER) to interact with genes different from those activated by ER bound to estradiol. Doming is a property often associated with, and considered a marker of, differentiation in mammary epithelial cells in culture. This study compared the ability of pure and partial agonist antiestrogens to stimulate doming. Materials and methods: MCF-7 cells grown in medium with 10% calf serum were treated with antiestrogens. Domes were counted in three rows (width of the 4× field) across the flask. Results: Three partial agonist antiestrogens [4-hydroxytamoxifen (OHT), H1285 and RU 39,411] caused dome formation. None of the pure antiestrogens tested (ICI 164,384, ICI 182,780 and RU 58,668) caused doming. Doming was stimulated in a dose-dependent manner starting at 1 nM OHT with maximum stimulation at 10–100 nM. Estradiol did not stimulate doming, but blocked doming at 1%–10% of the OHT concentration. Trichostatin A (TSA) reduced the level of estrogen receptor alpha (ERα) and adding it 24 h before adding OHT prevented dome formation. Conclusions: OHT and the other partial agonist antiestrogens appear to act through the ER to stimulate doming. The ability of tamoxifen to induce a marker of differentiation may play a role in its inhibition of breast tumors. If so, then the fact that other partial agonist antiestrogens share this ability, but that pure antiestrogens lack it, may be an important consideration in developing new antiestrogens for breast cancer therapy. Walter de Gruyter Online Zeitschriften antiestrogens breast cancer differentiation doming MCF-7 Butler, W. Barkley oth D’Amico, Stephen C. oth Glassford, William J. oth Wu, Weizhen oth Enthalten in Hormone molecular biology and clinical investigation Berlin : de Gruyter, 2010 12(2012), 3 vom: 05. Dez., Seite 419-423 (DE-627)NLEJ248235699 (DE-600)2536635-X 1868-1891 nnns volume:12 year:2012 number:3 day:05 month:12 pages:419-423 extent:5 https://doi.org/10.1515/hmbci-2012-0034 Deutschlandweit zugänglich GBV_USEFLAG_U ZDB-1-DGR GBV_NL_ARTICLE AR 12 2012 3 05 12 419-423 5 |
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10.1515/hmbci-2012-0034 doi artikel_Grundlieferung.pp (DE-627)NLEJ246929286 DE-627 ger DE-627 rakwb Partial agonist, but not pure antiestrogens stimulate doming, a marker of normal differentiation, in the MCF-7 breast cancer cell line De Gruyter 2012 5 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background: The mechanisms by which tamoxifen inhibits breast tumor growth are not completely understood. Partial agonist antiestrogens such as tamoxifen may cause the estrogen receptor (ER) to interact with genes different from those activated by ER bound to estradiol. Doming is a property often associated with, and considered a marker of, differentiation in mammary epithelial cells in culture. This study compared the ability of pure and partial agonist antiestrogens to stimulate doming. Materials and methods: MCF-7 cells grown in medium with 10% calf serum were treated with antiestrogens. Domes were counted in three rows (width of the 4× field) across the flask. Results: Three partial agonist antiestrogens [4-hydroxytamoxifen (OHT), H1285 and RU 39,411] caused dome formation. None of the pure antiestrogens tested (ICI 164,384, ICI 182,780 and RU 58,668) caused doming. Doming was stimulated in a dose-dependent manner starting at 1 nM OHT with maximum stimulation at 10–100 nM. Estradiol did not stimulate doming, but blocked doming at 1%–10% of the OHT concentration. Trichostatin A (TSA) reduced the level of estrogen receptor alpha (ERα) and adding it 24 h before adding OHT prevented dome formation. Conclusions: OHT and the other partial agonist antiestrogens appear to act through the ER to stimulate doming. The ability of tamoxifen to induce a marker of differentiation may play a role in its inhibition of breast tumors. If so, then the fact that other partial agonist antiestrogens share this ability, but that pure antiestrogens lack it, may be an important consideration in developing new antiestrogens for breast cancer therapy. Walter de Gruyter Online Zeitschriften antiestrogens breast cancer differentiation doming MCF-7 Butler, W. Barkley oth D’Amico, Stephen C. oth Glassford, William J. oth Wu, Weizhen oth Enthalten in Hormone molecular biology and clinical investigation Berlin : de Gruyter, 2010 12(2012), 3 vom: 05. Dez., Seite 419-423 (DE-627)NLEJ248235699 (DE-600)2536635-X 1868-1891 nnns volume:12 year:2012 number:3 day:05 month:12 pages:419-423 extent:5 https://doi.org/10.1515/hmbci-2012-0034 Deutschlandweit zugänglich GBV_USEFLAG_U ZDB-1-DGR GBV_NL_ARTICLE AR 12 2012 3 05 12 419-423 5 |
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Partial agonist, but not pure antiestrogens stimulate doming, a marker of normal differentiation, in the MCF-7 breast cancer cell line |
| abstract |
Background: The mechanisms by which tamoxifen inhibits breast tumor growth are not completely understood. Partial agonist antiestrogens such as tamoxifen may cause the estrogen receptor (ER) to interact with genes different from those activated by ER bound to estradiol. Doming is a property often associated with, and considered a marker of, differentiation in mammary epithelial cells in culture. This study compared the ability of pure and partial agonist antiestrogens to stimulate doming. Materials and methods: MCF-7 cells grown in medium with 10% calf serum were treated with antiestrogens. Domes were counted in three rows (width of the 4× field) across the flask. Results: Three partial agonist antiestrogens [4-hydroxytamoxifen (OHT), H1285 and RU 39,411] caused dome formation. None of the pure antiestrogens tested (ICI 164,384, ICI 182,780 and RU 58,668) caused doming. Doming was stimulated in a dose-dependent manner starting at 1 nM OHT with maximum stimulation at 10–100 nM. Estradiol did not stimulate doming, but blocked doming at 1%–10% of the OHT concentration. Trichostatin A (TSA) reduced the level of estrogen receptor alpha (ERα) and adding it 24 h before adding OHT prevented dome formation. Conclusions: OHT and the other partial agonist antiestrogens appear to act through the ER to stimulate doming. The ability of tamoxifen to induce a marker of differentiation may play a role in its inhibition of breast tumors. If so, then the fact that other partial agonist antiestrogens share this ability, but that pure antiestrogens lack it, may be an important consideration in developing new antiestrogens for breast cancer therapy. |
| abstractGer |
Background: The mechanisms by which tamoxifen inhibits breast tumor growth are not completely understood. Partial agonist antiestrogens such as tamoxifen may cause the estrogen receptor (ER) to interact with genes different from those activated by ER bound to estradiol. Doming is a property often associated with, and considered a marker of, differentiation in mammary epithelial cells in culture. This study compared the ability of pure and partial agonist antiestrogens to stimulate doming. Materials and methods: MCF-7 cells grown in medium with 10% calf serum were treated with antiestrogens. Domes were counted in three rows (width of the 4× field) across the flask. Results: Three partial agonist antiestrogens [4-hydroxytamoxifen (OHT), H1285 and RU 39,411] caused dome formation. None of the pure antiestrogens tested (ICI 164,384, ICI 182,780 and RU 58,668) caused doming. Doming was stimulated in a dose-dependent manner starting at 1 nM OHT with maximum stimulation at 10–100 nM. Estradiol did not stimulate doming, but blocked doming at 1%–10% of the OHT concentration. Trichostatin A (TSA) reduced the level of estrogen receptor alpha (ERα) and adding it 24 h before adding OHT prevented dome formation. Conclusions: OHT and the other partial agonist antiestrogens appear to act through the ER to stimulate doming. The ability of tamoxifen to induce a marker of differentiation may play a role in its inhibition of breast tumors. If so, then the fact that other partial agonist antiestrogens share this ability, but that pure antiestrogens lack it, may be an important consideration in developing new antiestrogens for breast cancer therapy. |
| abstract_unstemmed |
Background: The mechanisms by which tamoxifen inhibits breast tumor growth are not completely understood. Partial agonist antiestrogens such as tamoxifen may cause the estrogen receptor (ER) to interact with genes different from those activated by ER bound to estradiol. Doming is a property often associated with, and considered a marker of, differentiation in mammary epithelial cells in culture. This study compared the ability of pure and partial agonist antiestrogens to stimulate doming. Materials and methods: MCF-7 cells grown in medium with 10% calf serum were treated with antiestrogens. Domes were counted in three rows (width of the 4× field) across the flask. Results: Three partial agonist antiestrogens [4-hydroxytamoxifen (OHT), H1285 and RU 39,411] caused dome formation. None of the pure antiestrogens tested (ICI 164,384, ICI 182,780 and RU 58,668) caused doming. Doming was stimulated in a dose-dependent manner starting at 1 nM OHT with maximum stimulation at 10–100 nM. Estradiol did not stimulate doming, but blocked doming at 1%–10% of the OHT concentration. Trichostatin A (TSA) reduced the level of estrogen receptor alpha (ERα) and adding it 24 h before adding OHT prevented dome formation. Conclusions: OHT and the other partial agonist antiestrogens appear to act through the ER to stimulate doming. The ability of tamoxifen to induce a marker of differentiation may play a role in its inhibition of breast tumors. If so, then the fact that other partial agonist antiestrogens share this ability, but that pure antiestrogens lack it, may be an important consideration in developing new antiestrogens for breast cancer therapy. |
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| title_short |
Partial agonist, but not pure antiestrogens stimulate doming, a marker of normal differentiation, in the MCF-7 breast cancer cell line |
| url |
https://doi.org/10.1515/hmbci-2012-0034 |
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Butler, W. Barkley D’Amico, Stephen C. Glassford, William J. Wu, Weizhen |
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10.1515/hmbci-2012-0034 |
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2024-07-06T09:37:09.345Z |
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