Endothelial induced EMT in breast epithelial cells with stem cell properties
Epithelial to mesenchymal transition (EMT) is a critical event in cancer progression and is closely linked to the breast epithelial cancer stem cell phenotype. Given the close interaction between the vascular endothelium and cancer cells, especially at the invasive front, we asked whether endothelia...
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| Veröffentlicht in: | PloS one 2011-09, Vol.6 (9), p.e23833-e23833 |
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| creator | Sigurdsson, Valgardur Hilmarsdottir, Bylgja Sigmundsdottir, Hekla Fridriksdottir, Agla J R Ringnér, Markus Villadsen, Rene Borg, Ake Agnarsson, Bjarni A Petersen, Ole William Magnusson, Magnus K Gudjonsson, Thorarinn |
| description | Epithelial to mesenchymal transition (EMT) is a critical event in cancer progression and is closely linked to the breast epithelial cancer stem cell phenotype. Given the close interaction between the vascular endothelium and cancer cells, especially at the invasive front, we asked whether endothelial cells might play a role in EMT. Using a 3D culture model we demonstrate that endothelial cells are potent inducers of EMT in D492 an immortalized breast epithelial cell line with stem cell properties. Endothelial induced mesenchymal-like cells (D492M) derived from D492, show reduced expression of keratins, a switch from E-Cadherin (E-Cad) to N-Cadherin (N-Cad) and enhanced migration. Acquisition of cancer stem cell associated characteristics like increased CD44(high)/CD24(low) ratio, resistance to apoptosis and anchorage independent growth was also seen in D492M cells. Endothelial induced EMT in D492 was partially blocked by inhibition of HGF signaling. Basal-like breast cancer, a vascular rich cancer with stem cell properties and adverse prognosis has been linked with EMT. We immunostained several basal-like breast cancer samples for endothelial and EMT markers. Cancer cells close to the vascular rich areas show no or decreased expression of E-Cad and increased N-Cad expression suggesting EMT. Collectively, we have shown in a 3D culture model that endothelial cells are potent inducers of EMT in breast epithelial cells with stem cell properties. Furthermore, we demonstrate that basal-like breast cancer contains cells with an EMT phenotype, most prominently close to vascular rich areas of these tumors. We conclude that endothelial cells are potent inducers of EMT and may play a role in progression of basal-like breast cancer. |
| doi_str_mv | 10.1371/journal.pone.0023833 |
| format | Article |
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Given the close interaction between the vascular endothelium and cancer cells, especially at the invasive front, we asked whether endothelial cells might play a role in EMT. Using a 3D culture model we demonstrate that endothelial cells are potent inducers of EMT in D492 an immortalized breast epithelial cell line with stem cell properties. Endothelial induced mesenchymal-like cells (D492M) derived from D492, show reduced expression of keratins, a switch from E-Cadherin (E-Cad) to N-Cadherin (N-Cad) and enhanced migration. Acquisition of cancer stem cell associated characteristics like increased CD44(high)/CD24(low) ratio, resistance to apoptosis and anchorage independent growth was also seen in D492M cells. Endothelial induced EMT in D492 was partially blocked by inhibition of HGF signaling. Basal-like breast cancer, a vascular rich cancer with stem cell properties and adverse prognosis has been linked with EMT. We immunostained several basal-like breast cancer samples for endothelial and EMT markers. Cancer cells close to the vascular rich areas show no or decreased expression of E-Cad and increased N-Cad expression suggesting EMT. Collectively, we have shown in a 3D culture model that endothelial cells are potent inducers of EMT in breast epithelial cells with stem cell properties. Furthermore, we demonstrate that basal-like breast cancer contains cells with an EMT phenotype, most prominently close to vascular rich areas of these tumors. We conclude that endothelial cells are potent inducers of EMT and may play a role in progression of basal-like breast cancer.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0023833</identifier><identifier>PMID: 21915264</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Analysis ; Angiogenesis ; Apoptosis ; Apoptosis - physiology ; Biology ; Blotting, Western ; Breast cancer ; Cancer ; Cancer and Oncology ; Cancer och onkologi ; Cell culture ; Cell Dedifferentiation ; Cell Line ; Cell Line, Tumor ; Cells, Cultured ; Clinical Medicine ; E-cadherin ; Endothelial cells ; Endothelium ; Epidermal growth factor ; Epidermal Growth Factor - metabolism ; Epithelial cells ; Epithelial Cells - cytology ; Epithelial Cells - metabolism ; Epithelial-Mesenchymal Transition ; Female ; Fibroblast Growth Factors - metabolism ; Fibroblasts ; Flow Cytometry ; Genotype & phenotype ; Health sciences ; Hematology ; Hepatocyte Growth Factor - metabolism ; Hospitals ; Humans ; Hypoxia ; Immunochemistry ; In Vitro Techniques ; Invasiveness ; Keratin ; Klinisk medicin ; Laboratories ; Liver cancer ; Medical and Health Sciences ; Medical research ; Medicin och hälsovetenskap ; Medicine ; Mesenchyme ; Metastasis ; Morphogenesis ; N-Cadherin ; Neoplastic Stem Cells - cytology ; Neoplastic Stem Cells - metabolism ; Properties (attributes) ; Rodents ; Signaling ; Stem cells ; Three dimensional models ; Transforming Growth Factor beta1 - metabolism ; Tumors ; Vascular endothelial growth factor</subject><ispartof>PloS one, 2011-09, Vol.6 (9), p.e23833-e23833</ispartof><rights>COPYRIGHT 2011 Public Library of Science</rights><rights>2011 Sigurdsson 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>Sigurdsson et al. 2011</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c760t-9f78b9c6def842aa50c94aea945c78661e94868abc3ecc0a14128da6647edfef3</citedby><cites>FETCH-LOGICAL-c760t-9f78b9c6def842aa50c94aea945c78661e94868abc3ecc0a14128da6647edfef3</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/PMC3167828/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3167828/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,550,723,776,780,860,881,2096,2915,23845,27901,27902,53766,53768,79569,79570</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21915264$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://lup.lub.lu.se/record/2183627$$DView record from Swedish Publication Index$$Hfree_for_read</backlink></links><search><creatorcontrib>Sigurdsson, Valgardur</creatorcontrib><creatorcontrib>Hilmarsdottir, Bylgja</creatorcontrib><creatorcontrib>Sigmundsdottir, Hekla</creatorcontrib><creatorcontrib>Fridriksdottir, Agla J R</creatorcontrib><creatorcontrib>Ringnér, Markus</creatorcontrib><creatorcontrib>Villadsen, Rene</creatorcontrib><creatorcontrib>Borg, Ake</creatorcontrib><creatorcontrib>Agnarsson, Bjarni A</creatorcontrib><creatorcontrib>Petersen, Ole William</creatorcontrib><creatorcontrib>Magnusson, Magnus K</creatorcontrib><creatorcontrib>Gudjonsson, Thorarinn</creatorcontrib><title>Endothelial induced EMT in breast epithelial cells with stem cell properties</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Epithelial to mesenchymal transition (EMT) is a critical event in cancer progression and is closely linked to the breast epithelial cancer stem cell phenotype. Given the close interaction between the vascular endothelium and cancer cells, especially at the invasive front, we asked whether endothelial cells might play a role in EMT. Using a 3D culture model we demonstrate that endothelial cells are potent inducers of EMT in D492 an immortalized breast epithelial cell line with stem cell properties. Endothelial induced mesenchymal-like cells (D492M) derived from D492, show reduced expression of keratins, a switch from E-Cadherin (E-Cad) to N-Cadherin (N-Cad) and enhanced migration. Acquisition of cancer stem cell associated characteristics like increased CD44(high)/CD24(low) ratio, resistance to apoptosis and anchorage independent growth was also seen in D492M cells. Endothelial induced EMT in D492 was partially blocked by inhibition of HGF signaling. Basal-like breast cancer, a vascular rich cancer with stem cell properties and adverse prognosis has been linked with EMT. We immunostained several basal-like breast cancer samples for endothelial and EMT markers. Cancer cells close to the vascular rich areas show no or decreased expression of E-Cad and increased N-Cad expression suggesting EMT. Collectively, we have shown in a 3D culture model that endothelial cells are potent inducers of EMT in breast epithelial cells with stem cell properties. Furthermore, we demonstrate that basal-like breast cancer contains cells with an EMT phenotype, most prominently close to vascular rich areas of these tumors. We conclude that endothelial cells are potent inducers of EMT and may play a role in progression of basal-like breast cancer.</description><subject>Analysis</subject><subject>Angiogenesis</subject><subject>Apoptosis</subject><subject>Apoptosis - physiology</subject><subject>Biology</subject><subject>Blotting, Western</subject><subject>Breast cancer</subject><subject>Cancer</subject><subject>Cancer and Oncology</subject><subject>Cancer och onkologi</subject><subject>Cell culture</subject><subject>Cell Dedifferentiation</subject><subject>Cell Line</subject><subject>Cell Line, Tumor</subject><subject>Cells, Cultured</subject><subject>Clinical Medicine</subject><subject>E-cadherin</subject><subject>Endothelial cells</subject><subject>Endothelium</subject><subject>Epidermal growth factor</subject><subject>Epidermal Growth Factor - metabolism</subject><subject>Epithelial cells</subject><subject>Epithelial Cells - cytology</subject><subject>Epithelial Cells - metabolism</subject><subject>Epithelial-Mesenchymal Transition</subject><subject>Female</subject><subject>Fibroblast Growth Factors - metabolism</subject><subject>Fibroblasts</subject><subject>Flow Cytometry</subject><subject>Genotype & phenotype</subject><subject>Health sciences</subject><subject>Hematology</subject><subject>Hepatocyte Growth Factor - metabolism</subject><subject>Hospitals</subject><subject>Humans</subject><subject>Hypoxia</subject><subject>Immunochemistry</subject><subject>In Vitro Techniques</subject><subject>Invasiveness</subject><subject>Keratin</subject><subject>Klinisk medicin</subject><subject>Laboratories</subject><subject>Liver cancer</subject><subject>Medical and Health Sciences</subject><subject>Medical research</subject><subject>Medicin och hälsovetenskap</subject><subject>Medicine</subject><subject>Mesenchyme</subject><subject>Metastasis</subject><subject>Morphogenesis</subject><subject>N-Cadherin</subject><subject>Neoplastic Stem Cells - cytology</subject><subject>Neoplastic Stem Cells - metabolism</subject><subject>Properties (attributes)</subject><subject>Rodents</subject><subject>Signaling</subject><subject>Stem cells</subject><subject>Three dimensional models</subject><subject>Transforming Growth Factor beta1 - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>SwePub</collection><collection>SWEPUB Lunds universitet full text</collection><collection>SwePub Articles</collection><collection>SWEPUB Freely available online</collection><collection>SWEPUB Lunds universitet</collection><collection>SwePub Articles full text</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Sigurdsson, Valgardur</au><au>Hilmarsdottir, Bylgja</au><au>Sigmundsdottir, Hekla</au><au>Fridriksdottir, Agla J R</au><au>Ringnér, Markus</au><au>Villadsen, Rene</au><au>Borg, Ake</au><au>Agnarsson, Bjarni A</au><au>Petersen, Ole William</au><au>Magnusson, Magnus K</au><au>Gudjonsson, Thorarinn</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Endothelial induced EMT in breast epithelial cells with stem cell properties</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2011-09-06</date><risdate>2011</risdate><volume>6</volume><issue>9</issue><spage>e23833</spage><epage>e23833</epage><pages>e23833-e23833</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Epithelial to mesenchymal transition (EMT) is a critical event in cancer progression and is closely linked to the breast epithelial cancer stem cell phenotype. Given the close interaction between the vascular endothelium and cancer cells, especially at the invasive front, we asked whether endothelial cells might play a role in EMT. Using a 3D culture model we demonstrate that endothelial cells are potent inducers of EMT in D492 an immortalized breast epithelial cell line with stem cell properties. Endothelial induced mesenchymal-like cells (D492M) derived from D492, show reduced expression of keratins, a switch from E-Cadherin (E-Cad) to N-Cadherin (N-Cad) and enhanced migration. Acquisition of cancer stem cell associated characteristics like increased CD44(high)/CD24(low) ratio, resistance to apoptosis and anchorage independent growth was also seen in D492M cells. Endothelial induced EMT in D492 was partially blocked by inhibition of HGF signaling. Basal-like breast cancer, a vascular rich cancer with stem cell properties and adverse prognosis has been linked with EMT. We immunostained several basal-like breast cancer samples for endothelial and EMT markers. Cancer cells close to the vascular rich areas show no or decreased expression of E-Cad and increased N-Cad expression suggesting EMT. Collectively, we have shown in a 3D culture model that endothelial cells are potent inducers of EMT in breast epithelial cells with stem cell properties. Furthermore, we demonstrate that basal-like breast cancer contains cells with an EMT phenotype, most prominently close to vascular rich areas of these tumors. We conclude that endothelial cells are potent inducers of EMT and may play a role in progression of basal-like breast cancer.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>21915264</pmid><doi>10.1371/journal.pone.0023833</doi><tpages>e23833</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1932-6203 |
| ispartof | PloS one, 2011-09, Vol.6 (9), p.e23833-e23833 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_1308442067 |
| source | Public Library of Science (PLoS) Journals Open Access; MEDLINE; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central; SWEPUB Freely available online; Free Full-Text Journals in Chemistry |
| subjects | Analysis Angiogenesis Apoptosis Apoptosis - physiology Biology Blotting, Western Breast cancer Cancer Cancer and Oncology Cancer och onkologi Cell culture Cell Dedifferentiation Cell Line Cell Line, Tumor Cells, Cultured Clinical Medicine E-cadherin Endothelial cells Endothelium Epidermal growth factor Epidermal Growth Factor - metabolism Epithelial cells Epithelial Cells - cytology Epithelial Cells - metabolism Epithelial-Mesenchymal Transition Female Fibroblast Growth Factors - metabolism Fibroblasts Flow Cytometry Genotype & phenotype Health sciences Hematology Hepatocyte Growth Factor - metabolism Hospitals Humans Hypoxia Immunochemistry In Vitro Techniques Invasiveness Keratin Klinisk medicin Laboratories Liver cancer Medical and Health Sciences Medical research Medicin och hälsovetenskap Medicine Mesenchyme Metastasis Morphogenesis N-Cadherin Neoplastic Stem Cells - cytology Neoplastic Stem Cells - metabolism Properties (attributes) Rodents Signaling Stem cells Three dimensional models Transforming Growth Factor beta1 - metabolism Tumors Vascular endothelial growth factor |
| title | Endothelial induced EMT in breast epithelial cells with stem cell properties |
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