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Coexpression and cross-regulation of the prolactin receptor and sex steroid hormone receptors in breast cancer
The sex steroid hormones and PRL interact synergistically to control the neoplastic growth of the mammary gland. The basis for this hormonal synergy is unknown, but may involve cellular coexpression of the sex steroid and PRL receptors, coupled with receptor cross-regulation. To examine this hypothe...
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Published in: | The journal of clinical endocrinology and metabolism 1997-11, Vol.82 (11), p.3692-3699 |
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container_title | The journal of clinical endocrinology and metabolism |
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creator | ORMANDY, C. J HALL, R. E MANNING, D. L ROBERTSON, J. F. R BLAMEY, R. W KELLY, P. A NICHOLSON, R. I SUTHERLAND, R. L |
description | The sex steroid hormones and PRL interact synergistically to control the neoplastic growth of the mammary gland. The basis for this hormonal synergy is unknown, but may involve cellular coexpression of the sex steroid and PRL receptors, coupled with receptor cross-regulation. To examine this hypothesis the expression of the sex steroid and PRL receptors was examined in 20 human breast cancer cell lines and 123 primary breast cancers. Regulation of sex steroid receptors by PRL and of the PRL receptor by sex steroids was examined in T-47D and MCF-7 breast cancer cells. Northern analysis of the breast cancer cell lines and tumors indicated that the PRL receptor and the sex steroid receptors were coexpressed. The level of PRL receptor expression in the breast cancer cell lines was linearly related to that of the estrogen and progesterone receptors, but not to that of the androgen receptor. In MCF-7 and T-47D cells, acute treatment with progestins and androgens and long term treatment with estrogens increased PRL receptor levels. Analysis of sex steroid receptor messenger ribonucleic acid and binding activity showed that acute PRL treatment produced a time- and concentration-dependent increase in progesterone receptor and a decrease in androgen receptor. These results indicate that receptors for sex steroids and PRL are coexpressed and are cross-regulated, providing a potential mechanism for the observed synergy among estrogen, progesterone, and PRL in the control of tumor growth. |
doi_str_mv | 10.1210/jc.82.11.3692 |
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J ; HALL, R. E ; MANNING, D. L ; ROBERTSON, J. F. R ; BLAMEY, R. W ; KELLY, P. A ; NICHOLSON, R. I ; SUTHERLAND, R. L</creator><creatorcontrib>ORMANDY, C. J ; HALL, R. E ; MANNING, D. L ; ROBERTSON, J. F. R ; BLAMEY, R. W ; KELLY, P. A ; NICHOLSON, R. I ; SUTHERLAND, R. L</creatorcontrib><description>The sex steroid hormones and PRL interact synergistically to control the neoplastic growth of the mammary gland. The basis for this hormonal synergy is unknown, but may involve cellular coexpression of the sex steroid and PRL receptors, coupled with receptor cross-regulation. To examine this hypothesis the expression of the sex steroid and PRL receptors was examined in 20 human breast cancer cell lines and 123 primary breast cancers. Regulation of sex steroid receptors by PRL and of the PRL receptor by sex steroids was examined in T-47D and MCF-7 breast cancer cells. Northern analysis of the breast cancer cell lines and tumors indicated that the PRL receptor and the sex steroid receptors were coexpressed. The level of PRL receptor expression in the breast cancer cell lines was linearly related to that of the estrogen and progesterone receptors, but not to that of the androgen receptor. In MCF-7 and T-47D cells, acute treatment with progestins and androgens and long term treatment with estrogens increased PRL receptor levels. Analysis of sex steroid receptor messenger ribonucleic acid and binding activity showed that acute PRL treatment produced a time- and concentration-dependent increase in progesterone receptor and a decrease in androgen receptor. These results indicate that receptors for sex steroids and PRL are coexpressed and are cross-regulated, providing a potential mechanism for the observed synergy among estrogen, progesterone, and PRL in the control of tumor growth.</description><identifier>ISSN: 0021-972X</identifier><identifier>EISSN: 1945-7197</identifier><identifier>DOI: 10.1210/jc.82.11.3692</identifier><identifier>PMID: 9360527</identifier><identifier>CODEN: JCEMAZ</identifier><language>eng</language><publisher>Bethesda, MD: Endocrine Society</publisher><subject>Biological and medical sciences ; Blotting, Northern ; Breast Neoplasms - genetics ; Dihydrotestosterone - pharmacology ; Estradiol - pharmacology ; Female ; Gene Expression Regulation, Neoplastic - drug effects ; Gynecology. Andrology. Obstetrics ; Humans ; Mammary gland diseases ; Medical sciences ; Progesterone - pharmacology ; Prolactin - pharmacology ; Receptors, Androgen - genetics ; Receptors, Estrogen - genetics ; Receptors, Progesterone - genetics ; Receptors, Prolactin - genetics ; Receptors, Steroid - genetics ; Tumor Cells, Cultured ; Tumors</subject><ispartof>The journal of clinical endocrinology and metabolism, 1997-11, Vol.82 (11), p.3692-3699</ispartof><rights>1998 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c317t-262b6fc1c6a987b0ec968f5ff95bfc55dd077a6afa842d0b645927ba3a0cce473</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27923,27924</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=2051482$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9360527$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>ORMANDY, C. J</creatorcontrib><creatorcontrib>HALL, R. E</creatorcontrib><creatorcontrib>MANNING, D. L</creatorcontrib><creatorcontrib>ROBERTSON, J. F. R</creatorcontrib><creatorcontrib>BLAMEY, R. W</creatorcontrib><creatorcontrib>KELLY, P. A</creatorcontrib><creatorcontrib>NICHOLSON, R. I</creatorcontrib><creatorcontrib>SUTHERLAND, R. L</creatorcontrib><title>Coexpression and cross-regulation of the prolactin receptor and sex steroid hormone receptors in breast cancer</title><title>The journal of clinical endocrinology and metabolism</title><addtitle>J Clin Endocrinol Metab</addtitle><description>The sex steroid hormones and PRL interact synergistically to control the neoplastic growth of the mammary gland. The basis for this hormonal synergy is unknown, but may involve cellular coexpression of the sex steroid and PRL receptors, coupled with receptor cross-regulation. To examine this hypothesis the expression of the sex steroid and PRL receptors was examined in 20 human breast cancer cell lines and 123 primary breast cancers. Regulation of sex steroid receptors by PRL and of the PRL receptor by sex steroids was examined in T-47D and MCF-7 breast cancer cells. Northern analysis of the breast cancer cell lines and tumors indicated that the PRL receptor and the sex steroid receptors were coexpressed. The level of PRL receptor expression in the breast cancer cell lines was linearly related to that of the estrogen and progesterone receptors, but not to that of the androgen receptor. In MCF-7 and T-47D cells, acute treatment with progestins and androgens and long term treatment with estrogens increased PRL receptor levels. Analysis of sex steroid receptor messenger ribonucleic acid and binding activity showed that acute PRL treatment produced a time- and concentration-dependent increase in progesterone receptor and a decrease in androgen receptor. These results indicate that receptors for sex steroids and PRL are coexpressed and are cross-regulated, providing a potential mechanism for the observed synergy among estrogen, progesterone, and PRL in the control of tumor growth.</description><subject>Biological and medical sciences</subject><subject>Blotting, Northern</subject><subject>Breast Neoplasms - genetics</subject><subject>Dihydrotestosterone - pharmacology</subject><subject>Estradiol - pharmacology</subject><subject>Female</subject><subject>Gene Expression Regulation, Neoplastic - drug effects</subject><subject>Gynecology. Andrology. Obstetrics</subject><subject>Humans</subject><subject>Mammary gland diseases</subject><subject>Medical sciences</subject><subject>Progesterone - pharmacology</subject><subject>Prolactin - pharmacology</subject><subject>Receptors, Androgen - genetics</subject><subject>Receptors, Estrogen - genetics</subject><subject>Receptors, Progesterone - genetics</subject><subject>Receptors, Prolactin - genetics</subject><subject>Receptors, Steroid - genetics</subject><subject>Tumor Cells, Cultured</subject><subject>Tumors</subject><issn>0021-972X</issn><issn>1945-7197</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1997</creationdate><recordtype>article</recordtype><recordid>eNo90M9LwzAUB_AgypzTo0chB_HWmqRN0hxl-AsGXhS8hTR9cR1tM5MW5n9vt5WdHrz34fHeF6FbSlLKKHnc2LRgKaVpJhQ7Q3Oqcp5IquQ5mhPCaKIk-75EVzFuCKF5zrMZmqlMEM7kHHVLD7ttgBhr32HTVdgGH2MS4GdoTL9veof7NeBt8I2xfd3hABa2vQ8HHmGHYw_B1xVe-9D6Dk4g4lGXAUzssTWdhXCNLpxpItxMdYG-Xp4_l2_J6uP1ffm0SmxGZZ8wwUrhLLXCqEKWBKwShePOKV46y3lVESmNMM4UOatIKXKumCxNZoi1kMtsgR6Oe8erfweIvW7raKFpTAd-iFqqnIisUCNMjvDwdgCnt6FuTfjTlOh9vnpjdcE0pXqf7-jvpsVD2UJ10lOg4_x-mptoTePC-HYdT4wRTvOCZf-rHYWJ</recordid><startdate>19971101</startdate><enddate>19971101</enddate><creator>ORMANDY, C. J</creator><creator>HALL, R. E</creator><creator>MANNING, D. L</creator><creator>ROBERTSON, J. F. R</creator><creator>BLAMEY, R. W</creator><creator>KELLY, P. A</creator><creator>NICHOLSON, R. I</creator><creator>SUTHERLAND, R. L</creator><general>Endocrine Society</general><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>7X8</scope></search><sort><creationdate>19971101</creationdate><title>Coexpression and cross-regulation of the prolactin receptor and sex steroid hormone receptors in breast cancer</title><author>ORMANDY, C. J ; HALL, R. E ; MANNING, D. L ; ROBERTSON, J. F. R ; BLAMEY, R. W ; KELLY, P. A ; NICHOLSON, R. I ; SUTHERLAND, R. 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Obstetrics</topic><topic>Humans</topic><topic>Mammary gland diseases</topic><topic>Medical sciences</topic><topic>Progesterone - pharmacology</topic><topic>Prolactin - pharmacology</topic><topic>Receptors, Androgen - genetics</topic><topic>Receptors, Estrogen - genetics</topic><topic>Receptors, Progesterone - genetics</topic><topic>Receptors, Prolactin - genetics</topic><topic>Receptors, Steroid - genetics</topic><topic>Tumor Cells, Cultured</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>ORMANDY, C. J</creatorcontrib><creatorcontrib>HALL, R. E</creatorcontrib><creatorcontrib>MANNING, D. L</creatorcontrib><creatorcontrib>ROBERTSON, J. F. R</creatorcontrib><creatorcontrib>BLAMEY, R. W</creatorcontrib><creatorcontrib>KELLY, P. A</creatorcontrib><creatorcontrib>NICHOLSON, R. I</creatorcontrib><creatorcontrib>SUTHERLAND, R. 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L</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Coexpression and cross-regulation of the prolactin receptor and sex steroid hormone receptors in breast cancer</atitle><jtitle>The journal of clinical endocrinology and metabolism</jtitle><addtitle>J Clin Endocrinol Metab</addtitle><date>1997-11-01</date><risdate>1997</risdate><volume>82</volume><issue>11</issue><spage>3692</spage><epage>3699</epage><pages>3692-3699</pages><issn>0021-972X</issn><eissn>1945-7197</eissn><coden>JCEMAZ</coden><abstract>The sex steroid hormones and PRL interact synergistically to control the neoplastic growth of the mammary gland. The basis for this hormonal synergy is unknown, but may involve cellular coexpression of the sex steroid and PRL receptors, coupled with receptor cross-regulation. To examine this hypothesis the expression of the sex steroid and PRL receptors was examined in 20 human breast cancer cell lines and 123 primary breast cancers. Regulation of sex steroid receptors by PRL and of the PRL receptor by sex steroids was examined in T-47D and MCF-7 breast cancer cells. Northern analysis of the breast cancer cell lines and tumors indicated that the PRL receptor and the sex steroid receptors were coexpressed. The level of PRL receptor expression in the breast cancer cell lines was linearly related to that of the estrogen and progesterone receptors, but not to that of the androgen receptor. In MCF-7 and T-47D cells, acute treatment with progestins and androgens and long term treatment with estrogens increased PRL receptor levels. Analysis of sex steroid receptor messenger ribonucleic acid and binding activity showed that acute PRL treatment produced a time- and concentration-dependent increase in progesterone receptor and a decrease in androgen receptor. 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subjects | Biological and medical sciences Blotting, Northern Breast Neoplasms - genetics Dihydrotestosterone - pharmacology Estradiol - pharmacology Female Gene Expression Regulation, Neoplastic - drug effects Gynecology. Andrology. Obstetrics Humans Mammary gland diseases Medical sciences Progesterone - pharmacology Prolactin - pharmacology Receptors, Androgen - genetics Receptors, Estrogen - genetics Receptors, Progesterone - genetics Receptors, Prolactin - genetics Receptors, Steroid - genetics Tumor Cells, Cultured Tumors |
title | Coexpression and cross-regulation of the prolactin receptor and sex steroid hormone receptors in breast cancer |
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