Insulin-like growth factor-1 signaling regulates miRNA expression in MCF-7 breast cancer cell line
In breast carcinomas, increased levels of insulin-like growth factor 1 (IGF-1) can act as a mitogen to augment tumorigenesis through the regulation of MAPK and AKT signaling pathways. Signaling through these two pathways allows IGF-1 to employ mechanisms that favor proliferation and cellular surviva...
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| Veröffentlicht in: | PloS one 2012-11, Vol.7 (11), p.e49067 |
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| creator | Martin, Elizabeth C Bratton, Melyssa R Zhu, Yun Rhodes, Lyndsay V Tilghman, Syreeta L Collins-Burow, Bridgette M Burow, Matthew E |
| description | In breast carcinomas, increased levels of insulin-like growth factor 1 (IGF-1) can act as a mitogen to augment tumorigenesis through the regulation of MAPK and AKT signaling pathways. Signaling through these two pathways allows IGF-1 to employ mechanisms that favor proliferation and cellular survival. Here we demonstrate a subset of previously described tumor suppressor and oncogenic microRNAs (miRNAs) that are under the direct regulation of IGF-1 signaling. Additionally, we show that the selective inhibition of either the MAPK or AKT pathways prior to IGF-1 stimulation prevents the expression of previously described tumor suppressor miRNAs that are family and cluster specific. Here we have defined, for the first time, specific miRNAs under the direct regulation of IGF-1 signaling in the estrogen receptor positive MCF-7 breast cancer cell line and demonstrate kinase signaling as a modulator of expression for a small subset of microRNAs. Taken together, these data give new insights into mechanisms governing IGF-1 signaling in breast cancer. |
| doi_str_mv | 10.1371/journal.pone.0049067 |
| format | Article |
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Signaling through these two pathways allows IGF-1 to employ mechanisms that favor proliferation and cellular survival. Here we demonstrate a subset of previously described tumor suppressor and oncogenic microRNAs (miRNAs) that are under the direct regulation of IGF-1 signaling. Additionally, we show that the selective inhibition of either the MAPK or AKT pathways prior to IGF-1 stimulation prevents the expression of previously described tumor suppressor miRNAs that are family and cluster specific. Here we have defined, for the first time, specific miRNAs under the direct regulation of IGF-1 signaling in the estrogen receptor positive MCF-7 breast cancer cell line and demonstrate kinase signaling as a modulator of expression for a small subset of microRNAs. Taken together, these data give new insights into mechanisms governing IGF-1 signaling in breast cancer.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0049067</identifier><identifier>PMID: 23226206</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>AKT protein ; Apoptosis ; Biology ; Breast cancer ; Breast carcinoma ; Breast Neoplasms - genetics ; Breast Neoplasms - metabolism ; Breast Neoplasms - pathology ; Cancer ; Carcinoma - genetics ; Carcinoma - metabolism ; Carcinoma - pathology ; Cell cycle ; Cell growth ; Cell Line, Tumor ; Cell Proliferation - drug effects ; Cell survival ; Cell Survival - drug effects ; Estrogens ; Female ; Gastric cancer ; Gene expression ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic - drug effects ; Hematology ; Humans ; Insulin ; Insulin-like growth factor I ; Insulin-Like Growth Factor I - genetics ; Insulin-Like Growth Factor I - metabolism ; Insulin-Like Growth Factor I - pharmacology ; Insulin-like growth factors ; Kinases ; Liver cancer ; MAP kinase ; Medical research ; Medicine ; Metastasis ; MicroRNA ; MicroRNAs ; MicroRNAs - genetics ; MicroRNAs - metabolism ; miRNA ; Mitogen-Activated Protein Kinase Kinases - antagonists & inhibitors ; Mitogen-Activated Protein Kinase Kinases - genetics ; Mitogen-Activated Protein Kinase Kinases - metabolism ; Oligonucleotide Array Sequence Analysis ; Oncology ; Pathways ; Protein Kinase Inhibitors - pharmacology ; Proteins ; Proto-Oncogene Proteins c-akt - antagonists & inhibitors ; Proto-Oncogene Proteins c-akt - genetics ; Proto-Oncogene Proteins c-akt - metabolism ; Real-Time Polymerase Chain Reaction ; Signal transduction ; Signal Transduction - drug effects ; Signaling ; Stomach cancer ; Tumor suppressor genes ; Tumorigenesis</subject><ispartof>PloS one, 2012-11, Vol.7 (11), p.e49067</ispartof><rights>COPYRIGHT 2012 Public Library of Science</rights><rights>2012 Martin et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: https://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2012 Martin et al 2012 Martin et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c692t-e4f89f6de0725b736f9628cda04062403663384dd5bacf5f01693707f734fd0e3</citedby><cites>FETCH-LOGICAL-c692t-e4f89f6de0725b736f9628cda04062403663384dd5bacf5f01693707f734fd0e3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3511482/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3511482/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,725,778,782,862,883,2098,2917,23853,27911,27912,53778,53780,79355,79356</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23226206$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Creighton, Chad</contributor><creatorcontrib>Martin, Elizabeth C</creatorcontrib><creatorcontrib>Bratton, Melyssa R</creatorcontrib><creatorcontrib>Zhu, Yun</creatorcontrib><creatorcontrib>Rhodes, Lyndsay V</creatorcontrib><creatorcontrib>Tilghman, Syreeta L</creatorcontrib><creatorcontrib>Collins-Burow, Bridgette M</creatorcontrib><creatorcontrib>Burow, Matthew E</creatorcontrib><title>Insulin-like growth factor-1 signaling regulates miRNA expression in MCF-7 breast cancer cell line</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>In breast carcinomas, increased levels of insulin-like growth factor 1 (IGF-1) can act as a mitogen to augment tumorigenesis through the regulation of MAPK and AKT signaling pathways. Signaling through these two pathways allows IGF-1 to employ mechanisms that favor proliferation and cellular survival. Here we demonstrate a subset of previously described tumor suppressor and oncogenic microRNAs (miRNAs) that are under the direct regulation of IGF-1 signaling. Additionally, we show that the selective inhibition of either the MAPK or AKT pathways prior to IGF-1 stimulation prevents the expression of previously described tumor suppressor miRNAs that are family and cluster specific. Here we have defined, for the first time, specific miRNAs under the direct regulation of IGF-1 signaling in the estrogen receptor positive MCF-7 breast cancer cell line and demonstrate kinase signaling as a modulator of expression for a small subset of microRNAs. Taken together, these data give new insights into mechanisms governing IGF-1 signaling in breast cancer.</description><subject>AKT protein</subject><subject>Apoptosis</subject><subject>Biology</subject><subject>Breast cancer</subject><subject>Breast carcinoma</subject><subject>Breast Neoplasms - genetics</subject><subject>Breast Neoplasms - metabolism</subject><subject>Breast Neoplasms - pathology</subject><subject>Cancer</subject><subject>Carcinoma - genetics</subject><subject>Carcinoma - metabolism</subject><subject>Carcinoma - pathology</subject><subject>Cell cycle</subject><subject>Cell growth</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation - drug effects</subject><subject>Cell survival</subject><subject>Cell Survival - drug effects</subject><subject>Estrogens</subject><subject>Female</subject><subject>Gastric cancer</subject><subject>Gene expression</subject><subject>Gene Expression Profiling</subject><subject>Gene Expression Regulation, Neoplastic - drug effects</subject><subject>Hematology</subject><subject>Humans</subject><subject>Insulin</subject><subject>Insulin-like growth factor I</subject><subject>Insulin-Like Growth Factor I - genetics</subject><subject>Insulin-Like Growth Factor I - metabolism</subject><subject>Insulin-Like Growth Factor I - pharmacology</subject><subject>Insulin-like growth factors</subject><subject>Kinases</subject><subject>Liver cancer</subject><subject>MAP kinase</subject><subject>Medical research</subject><subject>Medicine</subject><subject>Metastasis</subject><subject>MicroRNA</subject><subject>MicroRNAs</subject><subject>MicroRNAs - genetics</subject><subject>MicroRNAs - metabolism</subject><subject>miRNA</subject><subject>Mitogen-Activated Protein Kinase Kinases - antagonists & inhibitors</subject><subject>Mitogen-Activated Protein Kinase Kinases - genetics</subject><subject>Mitogen-Activated Protein Kinase Kinases - metabolism</subject><subject>Oligonucleotide Array Sequence Analysis</subject><subject>Oncology</subject><subject>Pathways</subject><subject>Protein Kinase Inhibitors - pharmacology</subject><subject>Proteins</subject><subject>Proto-Oncogene Proteins c-akt - antagonists & inhibitors</subject><subject>Proto-Oncogene Proteins c-akt - genetics</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>Real-Time Polymerase Chain Reaction</subject><subject>Signal transduction</subject><subject>Signal Transduction - drug effects</subject><subject>Signaling</subject><subject>Stomach cancer</subject><subject>Tumor suppressor genes</subject><subject>Tumorigenesis</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>DOA</sourceid><recordid>eNqNkl-L1DAUxYso7rr6DUQDguBDx6TJJO2LMAyuDqwurH9eQ5redDJmmjFJdf32Zp3uMgMKkoeG2985uRxOUTwleEaoIK83fgyDcrOdH2CGMWswF_eKU9LQquQVpvcP7ifFoxg3GM9pzfnD4qSiVZXn_LRoV0McnR1KZ78B6oP_mdbIKJ18KAmKts9P2KFHAfrRqQQRbe3VxwWC612AGK0fkB3Qh-V5KVAbQMWEtBo0BKTBOZS18Lh4YJSL8GT6nhVfzt9-Xr4vLy7frZaLi1LzpkolMFM3hneARTVvBeWm4VWtO4UZ5hXDlHNKa9Z181ZpMzeY8IYKLIygzHQY6FnxfO-7cz7KKZ4oCZ2THA3DOBOrPdF5tZG7YLcq_JJeWfln4EMvVUhWO5BCKdZ2QuuuxoxpqJkBxrAGwnSrBMteb6bXxnYLnYYhBeWOTI__DHYte_9D5nUIq6ts8GIyCP77CDH9Y-WJ6lXeyg7GZzO9tVHLBRO8aSjjJFOzv1D5dLC1OhfE2Dw_Erw6EmQmwXXq1RijXH26-n_28usx-_KAXYNyaR29G1MuSjwG2R7UwccYwNwlR7C86fdtGvKm33Lqd5Y9O0z9TnRbaPobjP70-A</recordid><startdate>20121130</startdate><enddate>20121130</enddate><creator>Martin, Elizabeth C</creator><creator>Bratton, Melyssa R</creator><creator>Zhu, Yun</creator><creator>Rhodes, Lyndsay V</creator><creator>Tilghman, Syreeta L</creator><creator>Collins-Burow, Bridgette M</creator><creator>Burow, Matthew E</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</general><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>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20121130</creationdate><title>Insulin-like growth factor-1 signaling regulates miRNA expression in MCF-7 breast cancer cell line</title><author>Martin, Elizabeth C ; Bratton, Melyssa R ; Zhu, Yun ; Rhodes, Lyndsay V ; Tilghman, Syreeta L ; Collins-Burow, Bridgette M ; Burow, Matthew E</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c692t-e4f89f6de0725b736f9628cda04062403663384dd5bacf5f01693707f734fd0e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>AKT protein</topic><topic>Apoptosis</topic><topic>Biology</topic><topic>Breast cancer</topic><topic>Breast carcinoma</topic><topic>Breast Neoplasms - genetics</topic><topic>Breast Neoplasms - metabolism</topic><topic>Breast Neoplasms - pathology</topic><topic>Cancer</topic><topic>Carcinoma - genetics</topic><topic>Carcinoma - metabolism</topic><topic>Carcinoma - pathology</topic><topic>Cell cycle</topic><topic>Cell growth</topic><topic>Cell Line, Tumor</topic><topic>Cell Proliferation - drug effects</topic><topic>Cell survival</topic><topic>Cell Survival - drug effects</topic><topic>Estrogens</topic><topic>Female</topic><topic>Gastric cancer</topic><topic>Gene expression</topic><topic>Gene Expression Profiling</topic><topic>Gene Expression Regulation, Neoplastic - drug effects</topic><topic>Hematology</topic><topic>Humans</topic><topic>Insulin</topic><topic>Insulin-like growth factor I</topic><topic>Insulin-Like Growth Factor I - genetics</topic><topic>Insulin-Like Growth Factor I - metabolism</topic><topic>Insulin-Like Growth Factor I - pharmacology</topic><topic>Insulin-like growth factors</topic><topic>Kinases</topic><topic>Liver cancer</topic><topic>MAP kinase</topic><topic>Medical research</topic><topic>Medicine</topic><topic>Metastasis</topic><topic>MicroRNA</topic><topic>MicroRNAs</topic><topic>MicroRNAs - 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Signaling through these two pathways allows IGF-1 to employ mechanisms that favor proliferation and cellular survival. Here we demonstrate a subset of previously described tumor suppressor and oncogenic microRNAs (miRNAs) that are under the direct regulation of IGF-1 signaling. Additionally, we show that the selective inhibition of either the MAPK or AKT pathways prior to IGF-1 stimulation prevents the expression of previously described tumor suppressor miRNAs that are family and cluster specific. Here we have defined, for the first time, specific miRNAs under the direct regulation of IGF-1 signaling in the estrogen receptor positive MCF-7 breast cancer cell line and demonstrate kinase signaling as a modulator of expression for a small subset of microRNAs. Taken together, these data give new insights into mechanisms governing IGF-1 signaling in breast cancer.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>23226206</pmid><doi>10.1371/journal.pone.0049067</doi><tpages>e49067</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1932-6203 |
| ispartof | PloS one, 2012-11, Vol.7 (11), p.e49067 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_1351067400 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Public Library of Science (PLoS); PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | AKT protein Apoptosis Biology Breast cancer Breast carcinoma Breast Neoplasms - genetics Breast Neoplasms - metabolism Breast Neoplasms - pathology Cancer Carcinoma - genetics Carcinoma - metabolism Carcinoma - pathology Cell cycle Cell growth Cell Line, Tumor Cell Proliferation - drug effects Cell survival Cell Survival - drug effects Estrogens Female Gastric cancer Gene expression Gene Expression Profiling Gene Expression Regulation, Neoplastic - drug effects Hematology Humans Insulin Insulin-like growth factor I Insulin-Like Growth Factor I - genetics Insulin-Like Growth Factor I - metabolism Insulin-Like Growth Factor I - pharmacology Insulin-like growth factors Kinases Liver cancer MAP kinase Medical research Medicine Metastasis MicroRNA MicroRNAs MicroRNAs - genetics MicroRNAs - metabolism miRNA Mitogen-Activated Protein Kinase Kinases - antagonists & inhibitors Mitogen-Activated Protein Kinase Kinases - genetics Mitogen-Activated Protein Kinase Kinases - metabolism Oligonucleotide Array Sequence Analysis Oncology Pathways Protein Kinase Inhibitors - pharmacology Proteins Proto-Oncogene Proteins c-akt - antagonists & inhibitors Proto-Oncogene Proteins c-akt - genetics Proto-Oncogene Proteins c-akt - metabolism Real-Time Polymerase Chain Reaction Signal transduction Signal Transduction - drug effects Signaling Stomach cancer Tumor suppressor genes Tumorigenesis |
| title | Insulin-like growth factor-1 signaling regulates miRNA expression in MCF-7 breast cancer cell line |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-15T19%3A26%3A40IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Insulin-like%20growth%20factor-1%20signaling%20regulates%20miRNA%20expression%20in%20MCF-7%20breast%20cancer%20cell%20line&rft.jtitle=PloS%20one&rft.au=Martin,%20Elizabeth%20C&rft.date=2012-11-30&rft.volume=7&rft.issue=11&rft.spage=e49067&rft.pages=e49067-&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0049067&rft_dat=%3Cgale_plos_%3EA476993461%3C/gale_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1351067400&rft_id=info:pmid/23226206&rft_galeid=A476993461&rft_doaj_id=oai_doaj_org_article_7aa4bd7ccd8044ce84fe440ce14cba74&rfr_iscdi=true |