Let-7 family miRNAs regulate estrogen receptor alpha signaling in estrogen receptor positive breast cancer
In order to understand how microRNAs (miRNAs) regulate breast cancer tumorigenesis, a miRNA expression microarray screening was performed using RNA from formalin-fixed paraffin-embedded (FFPE) breast tissues, which included benign ( n = 13), ductal carcinoma in situ (DCIS) ( n = 16), and invasive...
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| creator | Zhao, Yingchun Deng, Caishu Wang, Jiarui Xiao, Jing Gatalica, Zoran Recker, Robert R. Xiao, Gary Guishan |
| description | In order to understand how microRNAs (miRNAs) regulate breast cancer tumorigenesis, a miRNA expression microarray screening was performed using RNA from formalin-fixed paraffin-embedded (FFPE) breast tissues, which included benign (
n
= 13), ductal carcinoma in situ (DCIS) (
n
= 16), and invasive ductal carcinoma (IDC) (
n
= 15). Twenty-five differentially expressed miRNAs (
P
|
| doi_str_mv | 10.1007/s10549-010-0972-2 |
| format | Article |
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n
= 13), ductal carcinoma in situ (DCIS) (
n
= 16), and invasive ductal carcinoma (IDC) (
n
= 15). Twenty-five differentially expressed miRNAs (
P
< 0.01) were identified, of which let-7 family miRNAs were down-regulated in human breast cancer tissues at stages of DCIS and IDC compared to benign stage. We further found that there was an inverse correlation between ER-α expression and several members of let-7 family in the FFPE tissues. Next, we performed bioinformatics analysis and found that let-7 miRNA sequences match sequence in the 3′-UTR of estrogen receptor alpha (ER-α), suggesting ER-α may be a target of let-7, which was further confirmed by a number of experimental assays, including luciferase assay, protein expression, and mRNA expression. Overexpression of let-7 miRNAs in ER-positive breast cancer MCF7 cell line negatively affected ER-α activity. As expected, dampening of the ER-α signaling by let-7 miRNAs inhibited cell proliferation, and subsequently triggered the cell apoptotic process in MCF7 cells. In conclusion, our findings indicate a new regulatory mechanism of let-7 miRNAs in ER-α mediated cellular malignant growth of breast cancer.</description><identifier>ISSN: 0167-6806</identifier><identifier>EISSN: 1573-7217</identifier><identifier>DOI: 10.1007/s10549-010-0972-2</identifier><identifier>PMID: 20535543</identifier><identifier>CODEN: BCTRD6</identifier><language>eng</language><publisher>Boston: Springer US</publisher><subject>Apoptosis - genetics ; Base Sequence ; Biological and medical sciences ; Breast cancer ; Breast Neoplasms - genetics ; Breast Neoplasms - metabolism ; Cancer ; Cancer research ; Cancer therapies ; Care and treatment ; Cell Line, Tumor ; Cell Proliferation ; Comparative analysis ; Diagnosis ; Estrogen ; Estrogen Receptor alpha - metabolism ; Estrogens ; Female ; Formaldehyde ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic ; Gynecology. Andrology. Obstetrics ; Humans ; Luciferase ; Mammary gland diseases ; Medical sciences ; Medicine ; Medicine & Public Health ; MicroRNA ; MicroRNAs - genetics ; MicroRNAs - metabolism ; Oncology ; Phenols ; Preclinical Study ; Ribonucleic acid ; RNA ; Signal Transduction ; Tumors</subject><ispartof>Breast cancer research and treatment, 2011-05, Vol.127 (1), p.69-80</ispartof><rights>Springer Science+Business Media, LLC. 2010</rights><rights>2015 INIST-CNRS</rights><rights>COPYRIGHT 2011 Springer</rights><rights>Springer Science+Business Media, LLC. 2011</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c530t-5fd52f9d9794856e41c1a4a03c61e22a299315cfed640cae2f689ec6dd1938aa3</citedby><cites>FETCH-LOGICAL-c530t-5fd52f9d9794856e41c1a4a03c61e22a299315cfed640cae2f689ec6dd1938aa3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s10549-010-0972-2$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s10549-010-0972-2$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27922,27923,41486,42555,51317</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=24099321$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20535543$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhao, Yingchun</creatorcontrib><creatorcontrib>Deng, Caishu</creatorcontrib><creatorcontrib>Wang, Jiarui</creatorcontrib><creatorcontrib>Xiao, Jing</creatorcontrib><creatorcontrib>Gatalica, Zoran</creatorcontrib><creatorcontrib>Recker, Robert R.</creatorcontrib><creatorcontrib>Xiao, Gary Guishan</creatorcontrib><title>Let-7 family miRNAs regulate estrogen receptor alpha signaling in estrogen receptor positive breast cancer</title><title>Breast cancer research and treatment</title><addtitle>Breast Cancer Res Treat</addtitle><addtitle>Breast Cancer Res Treat</addtitle><description>In order to understand how microRNAs (miRNAs) regulate breast cancer tumorigenesis, a miRNA expression microarray screening was performed using RNA from formalin-fixed paraffin-embedded (FFPE) breast tissues, which included benign (
n
= 13), ductal carcinoma in situ (DCIS) (
n
= 16), and invasive ductal carcinoma (IDC) (
n
= 15). Twenty-five differentially expressed miRNAs (
P
< 0.01) were identified, of which let-7 family miRNAs were down-regulated in human breast cancer tissues at stages of DCIS and IDC compared to benign stage. We further found that there was an inverse correlation between ER-α expression and several members of let-7 family in the FFPE tissues. Next, we performed bioinformatics analysis and found that let-7 miRNA sequences match sequence in the 3′-UTR of estrogen receptor alpha (ER-α), suggesting ER-α may be a target of let-7, which was further confirmed by a number of experimental assays, including luciferase assay, protein expression, and mRNA expression. Overexpression of let-7 miRNAs in ER-positive breast cancer MCF7 cell line negatively affected ER-α activity. As expected, dampening of the ER-α signaling by let-7 miRNAs inhibited cell proliferation, and subsequently triggered the cell apoptotic process in MCF7 cells. In conclusion, our findings indicate a new regulatory mechanism of let-7 miRNAs in ER-α mediated cellular malignant growth of breast cancer.</description><subject>Apoptosis - genetics</subject><subject>Base Sequence</subject><subject>Biological and medical sciences</subject><subject>Breast cancer</subject><subject>Breast Neoplasms - genetics</subject><subject>Breast Neoplasms - metabolism</subject><subject>Cancer</subject><subject>Cancer research</subject><subject>Cancer therapies</subject><subject>Care and treatment</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation</subject><subject>Comparative analysis</subject><subject>Diagnosis</subject><subject>Estrogen</subject><subject>Estrogen Receptor alpha - metabolism</subject><subject>Estrogens</subject><subject>Female</subject><subject>Formaldehyde</subject><subject>Gene Expression Profiling</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Gynecology. Andrology. Obstetrics</subject><subject>Humans</subject><subject>Luciferase</subject><subject>Mammary gland diseases</subject><subject>Medical sciences</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>MicroRNA</subject><subject>MicroRNAs - genetics</subject><subject>MicroRNAs - metabolism</subject><subject>Oncology</subject><subject>Phenols</subject><subject>Preclinical Study</subject><subject>Ribonucleic acid</subject><subject>RNA</subject><subject>Signal Transduction</subject><subject>Tumors</subject><issn>0167-6806</issn><issn>1573-7217</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNqFkl-L1DAUxYso7uzqB_BFiqI-dc3fpnkcFleFQUH0OdxNbzsZ0mZM2oX99mbs6LqyInkI3PzOTXLuKYpnlJxTQtTbRIkUuiKUVEQrVrEHxYpKxSvFqHpYrAitVVU3pD4pTlPaEZIpoh8XJ4xILqXgq2K3walSZQeD8zfl4L58WqcyYj97mLDENMXQ45grFvdTiCX4_RbK5PoRvBv70o33QPuQ3OSusbyKCGkqLYwW45PiUQc-4dPjflZ8u3z39eJDtfn8_uPFelNZyclUya6VrNOtVlo0skZBLQUBhNuaImPAtOZU2g7bWhALyLq60WjrtqWaNwD8rHiz9N3H8H3OrzODSxa9hxHDnIwmQjSUqvq_ZFNTqSnnNJMv_iJ3YY7Zg58QFYQpmaGXC9SDR-PGLkwR7KGlWWe7NddCqUyd30Pl1eLgbBixc7l-R_D6D8EWwU_bFPw8uTCmuyBdQBtDShE7s49ugHhjKDGHwJglMCYHxhwCY1jWPD9-bL4asP2t-JWQDLw6ApAs-C7mWbp0ywmS58EODrGFS_lo7DHeOvTv238AQwzVmA</recordid><startdate>20110501</startdate><enddate>20110501</enddate><creator>Zhao, Yingchun</creator><creator>Deng, Caishu</creator><creator>Wang, Jiarui</creator><creator>Xiao, Jing</creator><creator>Gatalica, Zoran</creator><creator>Recker, Robert R.</creator><creator>Xiao, Gary Guishan</creator><general>Springer US</general><general>Springer</general><general>Springer Nature B.V</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>3V.</scope><scope>7TO</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>K9-</scope><scope>K9.</scope><scope>M0R</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>7TM</scope></search><sort><creationdate>20110501</creationdate><title>Let-7 family miRNAs regulate estrogen receptor alpha signaling in estrogen receptor positive breast cancer</title><author>Zhao, Yingchun ; Deng, Caishu ; Wang, Jiarui ; Xiao, Jing ; Gatalica, Zoran ; Recker, Robert R. ; Xiao, Gary Guishan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c530t-5fd52f9d9794856e41c1a4a03c61e22a299315cfed640cae2f689ec6dd1938aa3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Apoptosis - genetics</topic><topic>Base Sequence</topic><topic>Biological and medical sciences</topic><topic>Breast cancer</topic><topic>Breast Neoplasms - genetics</topic><topic>Breast Neoplasms - metabolism</topic><topic>Cancer</topic><topic>Cancer research</topic><topic>Cancer therapies</topic><topic>Care and treatment</topic><topic>Cell Line, Tumor</topic><topic>Cell Proliferation</topic><topic>Comparative analysis</topic><topic>Diagnosis</topic><topic>Estrogen</topic><topic>Estrogen Receptor alpha - metabolism</topic><topic>Estrogens</topic><topic>Female</topic><topic>Formaldehyde</topic><topic>Gene Expression Profiling</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Gynecology. Andrology. Obstetrics</topic><topic>Humans</topic><topic>Luciferase</topic><topic>Mammary gland diseases</topic><topic>Medical sciences</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>MicroRNA</topic><topic>MicroRNAs - genetics</topic><topic>MicroRNAs - metabolism</topic><topic>Oncology</topic><topic>Phenols</topic><topic>Preclinical Study</topic><topic>Ribonucleic acid</topic><topic>RNA</topic><topic>Signal Transduction</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhao, Yingchun</creatorcontrib><creatorcontrib>Deng, Caishu</creatorcontrib><creatorcontrib>Wang, Jiarui</creatorcontrib><creatorcontrib>Xiao, Jing</creatorcontrib><creatorcontrib>Gatalica, Zoran</creatorcontrib><creatorcontrib>Recker, Robert R.</creatorcontrib><creatorcontrib>Xiao, Gary Guishan</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>ProQuest Central (Corporate)</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Consumer Health Database (Alumni Edition)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Consumer Health Database</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Research Library (Corporate)</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>Nucleic Acids Abstracts</collection><jtitle>Breast cancer research and treatment</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhao, Yingchun</au><au>Deng, Caishu</au><au>Wang, Jiarui</au><au>Xiao, Jing</au><au>Gatalica, Zoran</au><au>Recker, Robert R.</au><au>Xiao, Gary Guishan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Let-7 family miRNAs regulate estrogen receptor alpha signaling in estrogen receptor positive breast cancer</atitle><jtitle>Breast cancer research and treatment</jtitle><stitle>Breast Cancer Res Treat</stitle><addtitle>Breast Cancer Res Treat</addtitle><date>2011-05-01</date><risdate>2011</risdate><volume>127</volume><issue>1</issue><spage>69</spage><epage>80</epage><pages>69-80</pages><issn>0167-6806</issn><eissn>1573-7217</eissn><coden>BCTRD6</coden><abstract>In order to understand how microRNAs (miRNAs) regulate breast cancer tumorigenesis, a miRNA expression microarray screening was performed using RNA from formalin-fixed paraffin-embedded (FFPE) breast tissues, which included benign (
n
= 13), ductal carcinoma in situ (DCIS) (
n
= 16), and invasive ductal carcinoma (IDC) (
n
= 15). Twenty-five differentially expressed miRNAs (
P
< 0.01) were identified, of which let-7 family miRNAs were down-regulated in human breast cancer tissues at stages of DCIS and IDC compared to benign stage. We further found that there was an inverse correlation between ER-α expression and several members of let-7 family in the FFPE tissues. Next, we performed bioinformatics analysis and found that let-7 miRNA sequences match sequence in the 3′-UTR of estrogen receptor alpha (ER-α), suggesting ER-α may be a target of let-7, which was further confirmed by a number of experimental assays, including luciferase assay, protein expression, and mRNA expression. Overexpression of let-7 miRNAs in ER-positive breast cancer MCF7 cell line negatively affected ER-α activity. As expected, dampening of the ER-α signaling by let-7 miRNAs inhibited cell proliferation, and subsequently triggered the cell apoptotic process in MCF7 cells. In conclusion, our findings indicate a new regulatory mechanism of let-7 miRNAs in ER-α mediated cellular malignant growth of breast cancer.</abstract><cop>Boston</cop><pub>Springer US</pub><pmid>20535543</pmid><doi>10.1007/s10549-010-0972-2</doi><tpages>12</tpages></addata></record> |
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| subjects | Apoptosis - genetics Base Sequence Biological and medical sciences Breast cancer Breast Neoplasms - genetics Breast Neoplasms - metabolism Cancer Cancer research Cancer therapies Care and treatment Cell Line, Tumor Cell Proliferation Comparative analysis Diagnosis Estrogen Estrogen Receptor alpha - metabolism Estrogens Female Formaldehyde Gene Expression Profiling Gene Expression Regulation, Neoplastic Gynecology. Andrology. Obstetrics Humans Luciferase Mammary gland diseases Medical sciences Medicine Medicine & Public Health MicroRNA MicroRNAs - genetics MicroRNAs - metabolism Oncology Phenols Preclinical Study Ribonucleic acid RNA Signal Transduction Tumors |
| title | Let-7 family miRNAs regulate estrogen receptor alpha signaling in estrogen receptor positive breast cancer |
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