Estrogen-independent effects of ER-α36 in ER-negative breast cancer
► High expression of ER-α36 was observed in ER-negative breast cancers. ► ER-α36 was knocked down by artificial microRNA hairpins. ► Downregulation of ER-α36 sensitized cells to paclitaxel. ► Downregulation of ER-α36 decreased cell migration and invasion. Estrogen receptor-alpha 36 (ER-α36) is a var...
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| Veröffentlicht in: | Steroids 2012-05, Vol.77 (6), p.666-673 |
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| creator | Zhang, Jing Li, Guangliang Li, Zhongqi Yu, Xiongfei Zheng, Yi Jin, Ketao Wang, Haohao Gong, Yun Sun, Xiaoping Teng, Xiaodong Cao, Jiang Teng, Lisong |
| description | ► High expression of ER-α36 was observed in ER-negative breast cancers. ► ER-α36 was knocked down by artificial microRNA hairpins. ► Downregulation of ER-α36 sensitized cells to paclitaxel. ► Downregulation of ER-α36 decreased cell migration and invasion.
Estrogen receptor-alpha 36 (ER-α36) is a variant of ER-α that has been found to be expressed in conventional ER (ER-α66)-negative breast cancer cell lines and human breast cancer samples. In this study, we found that, using immunohistochemical study, ER-α36 expression was significantly higher in ER-negative tumors than in ER-positive tumors although the expression was not associated with other clinicopathological characteristics. We then constructed an ER-α36-specific microRNA hairpin vector and established stable ER-α36 knockdown cells, and found that the knockdown cells were more sensitive to paclitaxel; the c-Jun N-terminal kinase pathway appeared to be involved in the mechanism. Downregulation of ER-α36 also resulted in decreased migration and invasion. These changes were estrogen independent. Our findings indicated that target ER-α36 may be a strategy for treating ER-negative breast cancers. |
| doi_str_mv | 10.1016/j.steroids.2012.02.013 |
| format | Article |
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Estrogen receptor-alpha 36 (ER-α36) is a variant of ER-α that has been found to be expressed in conventional ER (ER-α66)-negative breast cancer cell lines and human breast cancer samples. In this study, we found that, using immunohistochemical study, ER-α36 expression was significantly higher in ER-negative tumors than in ER-positive tumors although the expression was not associated with other clinicopathological characteristics. We then constructed an ER-α36-specific microRNA hairpin vector and established stable ER-α36 knockdown cells, and found that the knockdown cells were more sensitive to paclitaxel; the c-Jun N-terminal kinase pathway appeared to be involved in the mechanism. Downregulation of ER-α36 also resulted in decreased migration and invasion. These changes were estrogen independent. Our findings indicated that target ER-α36 may be a strategy for treating ER-negative breast cancers.</description><identifier>ISSN: 0039-128X</identifier><identifier>EISSN: 1878-5867</identifier><identifier>DOI: 10.1016/j.steroids.2012.02.013</identifier><identifier>PMID: 22402113</identifier><identifier>CODEN: STEDAM</identifier><language>eng</language><publisher>Kidlington: Elsevier Inc</publisher><subject>Adult ; Biological and medical sciences ; Breast cancer ; Breast Neoplasms - drug therapy ; Breast Neoplasms - genetics ; Breast Neoplasms - metabolism ; Breast Neoplasms - pathology ; Cell Line, Tumor ; Cell Movement - drug effects ; Down-Regulation - drug effects ; Estrogen Receptor alpha - deficiency ; Estrogen Receptor alpha - genetics ; Estrogen Receptor alpha - metabolism ; Estrogen receptor-alpha 36 ; Estrogens - metabolism ; Female ; Fundamental and applied biological sciences. Psychology ; G2 Phase Cell Cycle Checkpoints - drug effects ; Gene Expression Regulation, Neoplastic - drug effects ; Gene Knockdown Techniques ; Gynecology. Andrology. Obstetrics ; Humans ; JNK Mitogen-Activated Protein Kinases - metabolism ; M Phase Cell Cycle Checkpoints - drug effects ; Mammary gland diseases ; Medical sciences ; Metastasis ; MicroRNAs - genetics ; Middle Aged ; Molecular Targeted Therapy ; Neoplasm Invasiveness ; Paclitaxel ; Paclitaxel - pharmacology ; Signal Transduction - drug effects ; Transfection ; Tumors ; Vertebrates: endocrinology</subject><ispartof>Steroids, 2012-05, Vol.77 (6), p.666-673</ispartof><rights>2012 Elsevier Inc.</rights><rights>2015 INIST-CNRS</rights><rights>Copyright © 2012 Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c313t-f0a070b80baeed5f8b6fc00f514ca1713215a2ddf5f4ff5ec2c2e2449eaea183</citedby><cites>FETCH-LOGICAL-c313t-f0a070b80baeed5f8b6fc00f514ca1713215a2ddf5f4ff5ec2c2e2449eaea183</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0039128X12000712$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3536,27903,27904,65309</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=25888045$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22402113$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhang, Jing</creatorcontrib><creatorcontrib>Li, Guangliang</creatorcontrib><creatorcontrib>Li, Zhongqi</creatorcontrib><creatorcontrib>Yu, Xiongfei</creatorcontrib><creatorcontrib>Zheng, Yi</creatorcontrib><creatorcontrib>Jin, Ketao</creatorcontrib><creatorcontrib>Wang, Haohao</creatorcontrib><creatorcontrib>Gong, Yun</creatorcontrib><creatorcontrib>Sun, Xiaoping</creatorcontrib><creatorcontrib>Teng, Xiaodong</creatorcontrib><creatorcontrib>Cao, Jiang</creatorcontrib><creatorcontrib>Teng, Lisong</creatorcontrib><title>Estrogen-independent effects of ER-α36 in ER-negative breast cancer</title><title>Steroids</title><addtitle>Steroids</addtitle><description>► High expression of ER-α36 was observed in ER-negative breast cancers. ► ER-α36 was knocked down by artificial microRNA hairpins. ► Downregulation of ER-α36 sensitized cells to paclitaxel. ► Downregulation of ER-α36 decreased cell migration and invasion.
Estrogen receptor-alpha 36 (ER-α36) is a variant of ER-α that has been found to be expressed in conventional ER (ER-α66)-negative breast cancer cell lines and human breast cancer samples. In this study, we found that, using immunohistochemical study, ER-α36 expression was significantly higher in ER-negative tumors than in ER-positive tumors although the expression was not associated with other clinicopathological characteristics. We then constructed an ER-α36-specific microRNA hairpin vector and established stable ER-α36 knockdown cells, and found that the knockdown cells were more sensitive to paclitaxel; the c-Jun N-terminal kinase pathway appeared to be involved in the mechanism. Downregulation of ER-α36 also resulted in decreased migration and invasion. These changes were estrogen independent. Our findings indicated that target ER-α36 may be a strategy for treating ER-negative breast cancers.</description><subject>Adult</subject><subject>Biological and medical sciences</subject><subject>Breast cancer</subject><subject>Breast Neoplasms - drug therapy</subject><subject>Breast Neoplasms - genetics</subject><subject>Breast Neoplasms - metabolism</subject><subject>Breast Neoplasms - pathology</subject><subject>Cell Line, Tumor</subject><subject>Cell Movement - drug effects</subject><subject>Down-Regulation - drug effects</subject><subject>Estrogen Receptor alpha - deficiency</subject><subject>Estrogen Receptor alpha - genetics</subject><subject>Estrogen Receptor alpha - metabolism</subject><subject>Estrogen receptor-alpha 36</subject><subject>Estrogens - metabolism</subject><subject>Female</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>G2 Phase Cell Cycle Checkpoints - drug effects</subject><subject>Gene Expression Regulation, Neoplastic - drug effects</subject><subject>Gene Knockdown Techniques</subject><subject>Gynecology. Andrology. Obstetrics</subject><subject>Humans</subject><subject>JNK Mitogen-Activated Protein Kinases - metabolism</subject><subject>M Phase Cell Cycle Checkpoints - drug effects</subject><subject>Mammary gland diseases</subject><subject>Medical sciences</subject><subject>Metastasis</subject><subject>MicroRNAs - genetics</subject><subject>Middle Aged</subject><subject>Molecular Targeted Therapy</subject><subject>Neoplasm Invasiveness</subject><subject>Paclitaxel</subject><subject>Paclitaxel - pharmacology</subject><subject>Signal Transduction - drug effects</subject><subject>Transfection</subject><subject>Tumors</subject><subject>Vertebrates: endocrinology</subject><issn>0039-128X</issn><issn>1878-5867</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkMtKAzEUhoMotl5eQWYjuJnxnGQu6U6p9QIFQVy4C5nMiaS0MzWZFnwsX8RnMqWtLoWfJIvvzzl8jF0gZAhYXs-y0JPvXBMyDsgziEFxwIYoK5kWsqwO2RBAjFLk8m3ATkKYAUApRvyYDTjPgSOKIbubhN5379Smrm1oSfFo-4SsJdOHpLPJ5CX9_hJl4trNs6V33bs1JbUnHfrE6NaQP2NHVs8Dne_uU_Z6P3kdP6bT54en8e00NQJFn1rQUEEtodZETWFlXVoDYAvMjcYKBcdC86axhc2tLchww4nn-Yg0aZTilF1tv1367mNFoVcLFwzN57qlbhUUAvBqJGIhouUWNb4LwZNVS-8W2n9GSG0EqpnaC1QbgQpiUMTixW7Gql5Q81vbG4vA5Q7Qwei59dGAC39cIaWEvIjczZajKGTtyKtgHEVbjfPRrWo6998uP6hjkpA</recordid><startdate>201205</startdate><enddate>201205</enddate><creator>Zhang, Jing</creator><creator>Li, Guangliang</creator><creator>Li, Zhongqi</creator><creator>Yu, Xiongfei</creator><creator>Zheng, Yi</creator><creator>Jin, Ketao</creator><creator>Wang, Haohao</creator><creator>Gong, Yun</creator><creator>Sun, Xiaoping</creator><creator>Teng, Xiaodong</creator><creator>Cao, Jiang</creator><creator>Teng, Lisong</creator><general>Elsevier Inc</general><general>Elsevier</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>201205</creationdate><title>Estrogen-independent effects of ER-α36 in ER-negative breast cancer</title><author>Zhang, Jing ; Li, Guangliang ; Li, Zhongqi ; Yu, Xiongfei ; Zheng, Yi ; Jin, Ketao ; Wang, Haohao ; Gong, Yun ; Sun, Xiaoping ; Teng, Xiaodong ; Cao, Jiang ; Teng, Lisong</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c313t-f0a070b80baeed5f8b6fc00f514ca1713215a2ddf5f4ff5ec2c2e2449eaea183</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Adult</topic><topic>Biological and medical sciences</topic><topic>Breast cancer</topic><topic>Breast Neoplasms - drug therapy</topic><topic>Breast Neoplasms - genetics</topic><topic>Breast Neoplasms - metabolism</topic><topic>Breast Neoplasms - pathology</topic><topic>Cell Line, Tumor</topic><topic>Cell Movement - drug effects</topic><topic>Down-Regulation - drug effects</topic><topic>Estrogen Receptor alpha - deficiency</topic><topic>Estrogen Receptor alpha - genetics</topic><topic>Estrogen Receptor alpha - metabolism</topic><topic>Estrogen receptor-alpha 36</topic><topic>Estrogens - metabolism</topic><topic>Female</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>G2 Phase Cell Cycle Checkpoints - drug effects</topic><topic>Gene Expression Regulation, Neoplastic - drug effects</topic><topic>Gene Knockdown Techniques</topic><topic>Gynecology. Andrology. Obstetrics</topic><topic>Humans</topic><topic>JNK Mitogen-Activated Protein Kinases - metabolism</topic><topic>M Phase Cell Cycle Checkpoints - drug effects</topic><topic>Mammary gland diseases</topic><topic>Medical sciences</topic><topic>Metastasis</topic><topic>MicroRNAs - genetics</topic><topic>Middle Aged</topic><topic>Molecular Targeted Therapy</topic><topic>Neoplasm Invasiveness</topic><topic>Paclitaxel</topic><topic>Paclitaxel - pharmacology</topic><topic>Signal Transduction - drug effects</topic><topic>Transfection</topic><topic>Tumors</topic><topic>Vertebrates: endocrinology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhang, Jing</creatorcontrib><creatorcontrib>Li, Guangliang</creatorcontrib><creatorcontrib>Li, Zhongqi</creatorcontrib><creatorcontrib>Yu, Xiongfei</creatorcontrib><creatorcontrib>Zheng, Yi</creatorcontrib><creatorcontrib>Jin, Ketao</creatorcontrib><creatorcontrib>Wang, Haohao</creatorcontrib><creatorcontrib>Gong, Yun</creatorcontrib><creatorcontrib>Sun, Xiaoping</creatorcontrib><creatorcontrib>Teng, Xiaodong</creatorcontrib><creatorcontrib>Cao, Jiang</creatorcontrib><creatorcontrib>Teng, Lisong</creatorcontrib><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>MEDLINE - Academic</collection><jtitle>Steroids</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhang, Jing</au><au>Li, Guangliang</au><au>Li, Zhongqi</au><au>Yu, Xiongfei</au><au>Zheng, Yi</au><au>Jin, Ketao</au><au>Wang, Haohao</au><au>Gong, Yun</au><au>Sun, Xiaoping</au><au>Teng, Xiaodong</au><au>Cao, Jiang</au><au>Teng, Lisong</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Estrogen-independent effects of ER-α36 in ER-negative breast cancer</atitle><jtitle>Steroids</jtitle><addtitle>Steroids</addtitle><date>2012-05</date><risdate>2012</risdate><volume>77</volume><issue>6</issue><spage>666</spage><epage>673</epage><pages>666-673</pages><issn>0039-128X</issn><eissn>1878-5867</eissn><coden>STEDAM</coden><abstract>► High expression of ER-α36 was observed in ER-negative breast cancers. ► ER-α36 was knocked down by artificial microRNA hairpins. ► Downregulation of ER-α36 sensitized cells to paclitaxel. ► Downregulation of ER-α36 decreased cell migration and invasion.
Estrogen receptor-alpha 36 (ER-α36) is a variant of ER-α that has been found to be expressed in conventional ER (ER-α66)-negative breast cancer cell lines and human breast cancer samples. In this study, we found that, using immunohistochemical study, ER-α36 expression was significantly higher in ER-negative tumors than in ER-positive tumors although the expression was not associated with other clinicopathological characteristics. We then constructed an ER-α36-specific microRNA hairpin vector and established stable ER-α36 knockdown cells, and found that the knockdown cells were more sensitive to paclitaxel; the c-Jun N-terminal kinase pathway appeared to be involved in the mechanism. Downregulation of ER-α36 also resulted in decreased migration and invasion. These changes were estrogen independent. Our findings indicated that target ER-α36 may be a strategy for treating ER-negative breast cancers.</abstract><cop>Kidlington</cop><pub>Elsevier Inc</pub><pmid>22402113</pmid><doi>10.1016/j.steroids.2012.02.013</doi><tpages>8</tpages></addata></record> |
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| subjects | Adult Biological and medical sciences Breast cancer Breast Neoplasms - drug therapy Breast Neoplasms - genetics Breast Neoplasms - metabolism Breast Neoplasms - pathology Cell Line, Tumor Cell Movement - drug effects Down-Regulation - drug effects Estrogen Receptor alpha - deficiency Estrogen Receptor alpha - genetics Estrogen Receptor alpha - metabolism Estrogen receptor-alpha 36 Estrogens - metabolism Female Fundamental and applied biological sciences. Psychology G2 Phase Cell Cycle Checkpoints - drug effects Gene Expression Regulation, Neoplastic - drug effects Gene Knockdown Techniques Gynecology. Andrology. Obstetrics Humans JNK Mitogen-Activated Protein Kinases - metabolism M Phase Cell Cycle Checkpoints - drug effects Mammary gland diseases Medical sciences Metastasis MicroRNAs - genetics Middle Aged Molecular Targeted Therapy Neoplasm Invasiveness Paclitaxel Paclitaxel - pharmacology Signal Transduction - drug effects Transfection Tumors Vertebrates: endocrinology |
| title | Estrogen-independent effects of ER-α36 in ER-negative breast cancer |
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