An integrated analysis to predict micro‐RNAs targeting both stemness and metastasis in breast cancer stem cells
Several evidences support the idea that a small population of tumour cells representing self‐renewal potential are involved in initiation, maintenance, metastasis, and outcomes of cancer therapy. Elucidation of microRNAs/genes regulatory networks activated in cancer stem cells (CSCs) is necessary fo...
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| Veröffentlicht in: | Journal of cellular and molecular medicine 2019-04, Vol.23 (4), p.2442-2456 |
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| container_title | Journal of cellular and molecular medicine |
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| creator | Rahimi, Mahsa Sharifi‐Zarchi, Ali Firouzi, Javad Azimi, Mahnaz Zarghami, Nosratollah Alizadeh, Effat Ebrahimi, Marzieh |
| description | Several evidences support the idea that a small population of tumour cells representing self‐renewal potential are involved in initiation, maintenance, metastasis, and outcomes of cancer therapy. Elucidation of microRNAs/genes regulatory networks activated in cancer stem cells (CSCs) is necessary for the identification of new targets for cancer therapy. The aim of the present study was to predict the miRNAs pattern, which can target both metastasis and self‐renewal pathways using integration of literature and data mining. For this purpose, mammospheres derived from MCF‐7, MDA‐MB231, and MDA‐MB468 were used as breast CSCs model. They had higher migration, invasion, and colony formation potential, with increasing in stemness‐ and EMT‐related genes expression. Our results determined that miR‐204, ‐200c, ‐34a, and ‐10b contemporarily could target both self‐renewal and EMT pathways. This core regulatory of miRNAs could increase the survival rate of breast invasive carcinoma via up‐regulation of OCT4, SOX2, KLF4, c‐MYC, NOTCH1, SNAI1, ZEB1, and CDH2 and down‐regulation of CDH1. The majority of those target genes were involved in the regulation of pluripotency, MAPK, WNT, Hedgehog, p53, and transforming growth factor β pathways. Hence, this study provides novel insights for targeting core regulatory of miRNAs in breast CSCs to target both self‐renewal and metastasis potential and eradication of breast cancer. |
| doi_str_mv | 10.1111/jcmm.14090 |
| format | Article |
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Elucidation of microRNAs/genes regulatory networks activated in cancer stem cells (CSCs) is necessary for the identification of new targets for cancer therapy. The aim of the present study was to predict the miRNAs pattern, which can target both metastasis and self‐renewal pathways using integration of literature and data mining. For this purpose, mammospheres derived from MCF‐7, MDA‐MB231, and MDA‐MB468 were used as breast CSCs model. They had higher migration, invasion, and colony formation potential, with increasing in stemness‐ and EMT‐related genes expression. Our results determined that miR‐204, ‐200c, ‐34a, and ‐10b contemporarily could target both self‐renewal and EMT pathways. This core regulatory of miRNAs could increase the survival rate of breast invasive carcinoma via up‐regulation of OCT4, SOX2, KLF4, c‐MYC, NOTCH1, SNAI1, ZEB1, and CDH2 and down‐regulation of CDH1. The majority of those target genes were involved in the regulation of pluripotency, MAPK, WNT, Hedgehog, p53, and transforming growth factor β pathways. Hence, this study provides novel insights for targeting core regulatory of miRNAs in breast CSCs to target both self‐renewal and metastasis potential and eradication of breast cancer.</description><identifier>ISSN: 1582-1838</identifier><identifier>EISSN: 1582-4934</identifier><identifier>DOI: 10.1111/jcmm.14090</identifier><identifier>PMID: 30710426</identifier><language>eng</language><publisher>England: John Wiley & Sons, Inc</publisher><subject>Breast cancer ; breast cancer stem cell ; Breast Neoplasms - genetics ; Breast Neoplasms - pathology ; Cancer therapies ; Cell adhesion & migration ; Cell Movement - genetics ; Cell Proliferation - genetics ; Cell self-renewal ; Data processing ; E-cadherin ; EMT ; Epithelial-Mesenchymal Transition - genetics ; Eradication ; Female ; Gene Expression Regulation, Neoplastic - genetics ; Genes ; Growth factors ; Humans ; Invasiveness ; KLF4 protein ; MAP kinase ; MCF-7 Cells ; Metastases ; Metastasis ; MicroRNAs ; MicroRNAs - classification ; MicroRNAs - genetics ; Migration ; miRNA ; miRNAs ; Myc protein ; Neoplasm Metastasis ; Neoplasm Proteins - classification ; Neoplasm Proteins - genetics ; Neoplastic Stem Cells - metabolism ; Neoplastic Stem Cells - pathology ; Oct-4 protein ; Original ; p53 Protein ; Pluripotency ; Regulation ; self‐renewal ; Snail protein ; Stem cells ; Transforming growth factor ; Transforming growth factor-b ; Tumors ; Wnt protein</subject><ispartof>Journal of cellular and molecular medicine, 2019-04, Vol.23 (4), p.2442-2456</ispartof><rights>2019 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine.</rights><rights>2019. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3910-9ff2e60a9c88ec2238e91000a601ea14d3f42b53fa91dba755c82b4ef8b8582a3</citedby><cites>FETCH-LOGICAL-c3910-9ff2e60a9c88ec2238e91000a601ea14d3f42b53fa91dba755c82b4ef8b8582a3</cites><orcidid>0000-0003-1140-0379</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6433858/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6433858/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,1411,11541,27901,27902,45550,45551,46027,46451,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30710426$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Rahimi, Mahsa</creatorcontrib><creatorcontrib>Sharifi‐Zarchi, Ali</creatorcontrib><creatorcontrib>Firouzi, Javad</creatorcontrib><creatorcontrib>Azimi, Mahnaz</creatorcontrib><creatorcontrib>Zarghami, Nosratollah</creatorcontrib><creatorcontrib>Alizadeh, Effat</creatorcontrib><creatorcontrib>Ebrahimi, Marzieh</creatorcontrib><title>An integrated analysis to predict micro‐RNAs targeting both stemness and metastasis in breast cancer stem cells</title><title>Journal of cellular and molecular medicine</title><addtitle>J Cell Mol Med</addtitle><description>Several evidences support the idea that a small population of tumour cells representing self‐renewal potential are involved in initiation, maintenance, metastasis, and outcomes of cancer therapy. Elucidation of microRNAs/genes regulatory networks activated in cancer stem cells (CSCs) is necessary for the identification of new targets for cancer therapy. The aim of the present study was to predict the miRNAs pattern, which can target both metastasis and self‐renewal pathways using integration of literature and data mining. For this purpose, mammospheres derived from MCF‐7, MDA‐MB231, and MDA‐MB468 were used as breast CSCs model. They had higher migration, invasion, and colony formation potential, with increasing in stemness‐ and EMT‐related genes expression. Our results determined that miR‐204, ‐200c, ‐34a, and ‐10b contemporarily could target both self‐renewal and EMT pathways. This core regulatory of miRNAs could increase the survival rate of breast invasive carcinoma via up‐regulation of OCT4, SOX2, KLF4, c‐MYC, NOTCH1, SNAI1, ZEB1, and CDH2 and down‐regulation of CDH1. The majority of those target genes were involved in the regulation of pluripotency, MAPK, WNT, Hedgehog, p53, and transforming growth factor β pathways. Hence, this study provides novel insights for targeting core regulatory of miRNAs in breast CSCs to target both self‐renewal and metastasis potential and eradication of breast cancer.</description><subject>Breast cancer</subject><subject>breast cancer stem cell</subject><subject>Breast Neoplasms - genetics</subject><subject>Breast Neoplasms - pathology</subject><subject>Cancer therapies</subject><subject>Cell adhesion & migration</subject><subject>Cell Movement - genetics</subject><subject>Cell Proliferation - genetics</subject><subject>Cell self-renewal</subject><subject>Data processing</subject><subject>E-cadherin</subject><subject>EMT</subject><subject>Epithelial-Mesenchymal Transition - genetics</subject><subject>Eradication</subject><subject>Female</subject><subject>Gene Expression Regulation, Neoplastic - genetics</subject><subject>Genes</subject><subject>Growth factors</subject><subject>Humans</subject><subject>Invasiveness</subject><subject>KLF4 protein</subject><subject>MAP kinase</subject><subject>MCF-7 Cells</subject><subject>Metastases</subject><subject>Metastasis</subject><subject>MicroRNAs</subject><subject>MicroRNAs - classification</subject><subject>MicroRNAs - genetics</subject><subject>Migration</subject><subject>miRNA</subject><subject>miRNAs</subject><subject>Myc protein</subject><subject>Neoplasm Metastasis</subject><subject>Neoplasm Proteins - classification</subject><subject>Neoplasm Proteins - genetics</subject><subject>Neoplastic Stem Cells - metabolism</subject><subject>Neoplastic Stem Cells - pathology</subject><subject>Oct-4 protein</subject><subject>Original</subject><subject>p53 Protein</subject><subject>Pluripotency</subject><subject>Regulation</subject><subject>self‐renewal</subject><subject>Snail protein</subject><subject>Stem cells</subject><subject>Transforming growth factor</subject><subject>Transforming growth factor-b</subject><subject>Tumors</subject><subject>Wnt protein</subject><issn>1582-1838</issn><issn>1582-4934</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp9kc1qGzEQx0VoyVdzyQMEQS-h4FSz0u5Kl4Ix_SRpobRnodXOOjK7WkeSE3zrI-QZ-ySVYzekPUQINBr95o9m_oScAruAvN4u7DBcgGCK7ZFDKGUxEYqLF7sYJJcH5CjGBWO8Aq72yQFnNTBRVIfkZuqp8wnnwSRsqfGmX0cXaRrpMmDrbKKDs2H8_ev--9dpzpswx-T8nDZjuqYx4eAxxlzY0gGTiXnncudpEzDfqDXeYngAqcW-j6_Iy870EU925zH5-eH9j9mnyeW3j59n08uJ5QrYRHVdgRUzykqJtii4xJxmzFQM0IBoeSeKpuSdUdA2pi5LK4tGYCcbmds2_Ji82-ouV82ArUWfgun1MrjBhLUejdP_vnh3refjra4E51kiC5zvBMJ4s8KY9ODipgXjcVxFXUCtSiHrqsro6__QxbgKeZaZEqViqlSSPUuBqhkoUCJTb7ZUnnqMAbvHLwPTG7_1xm_94HeGz542-Yj-NTgDsAXuXI_rZ6T0l9nV1Vb0Dxent40</recordid><startdate>201904</startdate><enddate>201904</enddate><creator>Rahimi, Mahsa</creator><creator>Sharifi‐Zarchi, Ali</creator><creator>Firouzi, Javad</creator><creator>Azimi, Mahnaz</creator><creator>Zarghami, Nosratollah</creator><creator>Alizadeh, Effat</creator><creator>Ebrahimi, Marzieh</creator><general>John Wiley & Sons, Inc</general><general>John Wiley and Sons Inc</general><scope>24P</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>7QP</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88I</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>P64</scope><scope>PHGZM</scope><scope>PHGZT</scope><scope>PIMPY</scope><scope>PJZUB</scope><scope>PKEHL</scope><scope>PPXIY</scope><scope>PQEST</scope><scope>PQGLB</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0003-1140-0379</orcidid></search><sort><creationdate>201904</creationdate><title>An integrated analysis to predict micro‐RNAs targeting both stemness and metastasis in breast cancer stem cells</title><author>Rahimi, Mahsa ; Sharifi‐Zarchi, Ali ; Firouzi, Javad ; Azimi, Mahnaz ; Zarghami, Nosratollah ; Alizadeh, Effat ; Ebrahimi, Marzieh</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3910-9ff2e60a9c88ec2238e91000a601ea14d3f42b53fa91dba755c82b4ef8b8582a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Breast cancer</topic><topic>breast cancer stem cell</topic><topic>Breast Neoplasms - genetics</topic><topic>Breast Neoplasms - pathology</topic><topic>Cancer therapies</topic><topic>Cell adhesion & migration</topic><topic>Cell Movement - genetics</topic><topic>Cell Proliferation - genetics</topic><topic>Cell self-renewal</topic><topic>Data processing</topic><topic>E-cadherin</topic><topic>EMT</topic><topic>Epithelial-Mesenchymal Transition - genetics</topic><topic>Eradication</topic><topic>Female</topic><topic>Gene Expression Regulation, Neoplastic - genetics</topic><topic>Genes</topic><topic>Growth factors</topic><topic>Humans</topic><topic>Invasiveness</topic><topic>KLF4 protein</topic><topic>MAP kinase</topic><topic>MCF-7 Cells</topic><topic>Metastases</topic><topic>Metastasis</topic><topic>MicroRNAs</topic><topic>MicroRNAs - classification</topic><topic>MicroRNAs - genetics</topic><topic>Migration</topic><topic>miRNA</topic><topic>miRNAs</topic><topic>Myc protein</topic><topic>Neoplasm Metastasis</topic><topic>Neoplasm Proteins - classification</topic><topic>Neoplasm Proteins - genetics</topic><topic>Neoplastic Stem Cells - metabolism</topic><topic>Neoplastic Stem Cells - pathology</topic><topic>Oct-4 protein</topic><topic>Original</topic><topic>p53 Protein</topic><topic>Pluripotency</topic><topic>Regulation</topic><topic>self‐renewal</topic><topic>Snail protein</topic><topic>Stem cells</topic><topic>Transforming growth factor</topic><topic>Transforming growth factor-b</topic><topic>Tumors</topic><topic>Wnt protein</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Rahimi, Mahsa</creatorcontrib><creatorcontrib>Sharifi‐Zarchi, Ali</creatorcontrib><creatorcontrib>Firouzi, Javad</creatorcontrib><creatorcontrib>Azimi, Mahnaz</creatorcontrib><creatorcontrib>Zarghami, Nosratollah</creatorcontrib><creatorcontrib>Alizadeh, Effat</creatorcontrib><creatorcontrib>Ebrahimi, Marzieh</creatorcontrib><collection>Wiley Online Library Open Access</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>Calcium & Calcified Tissue Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest Central (New)</collection><collection>ProQuest One Academic (New)</collection><collection>Publicly Available Content Database</collection><collection>ProQuest Health & Medical Research Collection</collection><collection>ProQuest One Academic Middle East (New)</collection><collection>ProQuest One Health & Nursing</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Applied & Life Sciences</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Journal of cellular and molecular medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Rahimi, Mahsa</au><au>Sharifi‐Zarchi, Ali</au><au>Firouzi, Javad</au><au>Azimi, Mahnaz</au><au>Zarghami, Nosratollah</au><au>Alizadeh, Effat</au><au>Ebrahimi, Marzieh</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>An integrated analysis to predict micro‐RNAs targeting both stemness and metastasis in breast cancer stem cells</atitle><jtitle>Journal of cellular and molecular medicine</jtitle><addtitle>J Cell Mol Med</addtitle><date>2019-04</date><risdate>2019</risdate><volume>23</volume><issue>4</issue><spage>2442</spage><epage>2456</epage><pages>2442-2456</pages><issn>1582-1838</issn><eissn>1582-4934</eissn><abstract>Several evidences support the idea that a small population of tumour cells representing self‐renewal potential are involved in initiation, maintenance, metastasis, and outcomes of cancer therapy. Elucidation of microRNAs/genes regulatory networks activated in cancer stem cells (CSCs) is necessary for the identification of new targets for cancer therapy. The aim of the present study was to predict the miRNAs pattern, which can target both metastasis and self‐renewal pathways using integration of literature and data mining. For this purpose, mammospheres derived from MCF‐7, MDA‐MB231, and MDA‐MB468 were used as breast CSCs model. They had higher migration, invasion, and colony formation potential, with increasing in stemness‐ and EMT‐related genes expression. Our results determined that miR‐204, ‐200c, ‐34a, and ‐10b contemporarily could target both self‐renewal and EMT pathways. This core regulatory of miRNAs could increase the survival rate of breast invasive carcinoma via up‐regulation of OCT4, SOX2, KLF4, c‐MYC, NOTCH1, SNAI1, ZEB1, and CDH2 and down‐regulation of CDH1. The majority of those target genes were involved in the regulation of pluripotency, MAPK, WNT, Hedgehog, p53, and transforming growth factor β pathways. Hence, this study provides novel insights for targeting core regulatory of miRNAs in breast CSCs to target both self‐renewal and metastasis potential and eradication of breast cancer.</abstract><cop>England</cop><pub>John Wiley & Sons, Inc</pub><pmid>30710426</pmid><doi>10.1111/jcmm.14090</doi><tpages>15</tpages><orcidid>https://orcid.org/0000-0003-1140-0379</orcidid><oa>free_for_read</oa></addata></record> |
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| ispartof | Journal of cellular and molecular medicine, 2019-04, Vol.23 (4), p.2442-2456 |
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| language | eng |
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| source | MEDLINE; Wiley Online Library Open Access; DOAJ Directory of Open Access Journals; Wiley Online Library Journals Frontfile Complete; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central |
| subjects | Breast cancer breast cancer stem cell Breast Neoplasms - genetics Breast Neoplasms - pathology Cancer therapies Cell adhesion & migration Cell Movement - genetics Cell Proliferation - genetics Cell self-renewal Data processing E-cadherin EMT Epithelial-Mesenchymal Transition - genetics Eradication Female Gene Expression Regulation, Neoplastic - genetics Genes Growth factors Humans Invasiveness KLF4 protein MAP kinase MCF-7 Cells Metastases Metastasis MicroRNAs MicroRNAs - classification MicroRNAs - genetics Migration miRNA miRNAs Myc protein Neoplasm Metastasis Neoplasm Proteins - classification Neoplasm Proteins - genetics Neoplastic Stem Cells - metabolism Neoplastic Stem Cells - pathology Oct-4 protein Original p53 Protein Pluripotency Regulation self‐renewal Snail protein Stem cells Transforming growth factor Transforming growth factor-b Tumors Wnt protein |
| title | An integrated analysis to predict micro‐RNAs targeting both stemness and metastasis in breast cancer stem cells |
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