YKL-40/CHI3L1 facilitates migration and invasion in HER2 overexpressing breast epithelial progenitor cells and generates a niche for capillary-like network formation.
To access publisher's full text version of this article, please click on the hyperlink in Additional Links field or click on the hyperlink at the top of the page marked Download Epithelial to mesenchymal transition (EMT) is a developmental event that is hijacked in some diseases such as fibrosi...
Published in: | In Vitro Cellular & Developmental Biology - Animal |
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ftlandspitaliuni:oai:www.hirsla.lsh.is:2336/621252 2023-05-15T16:49:08+02:00 YKL-40/CHI3L1 facilitates migration and invasion in HER2 overexpressing breast epithelial progenitor cells and generates a niche for capillary-like network formation. Morera, Erika Steinhäuser, Sarah Sophie Budkova, Zuzana Ingthorsson, Saevar Kricker, Jennifer Krueger, Aileen Traustadottir, Gunnhildur Asta Gudjonsson, Thorarinn 1 Stem Cell Research Unit, Biomedical Center, Department of Anatomy, Faculty of Medicine, School of Health Sciences, University of Iceland, Vatnsmyrarvegi 16, 101, Reykjavik, Iceland. 2 Heidelberg Institute for Stem Cell Technology and Experimental Medicine, Heidelberg, Germany. 3 Stem Cell Research Unit, Biomedical Center, Department of Anatomy, Faculty of Medicine, School of Health Sciences, University of Iceland, Vatnsmyrarvegi 16, 101, Reykjavik, Iceland. tgudjons@hi.is. 4 Department of Laboratory Hematology, Landspitali - University Hospital, Reykjavik, Iceland. tgudjons@hi.is. 2019-12 http://hdl.handle.net/2336/621252 https://doi.org/10.1007/s11626-019-00403-x en eng Springer https://link.springer.com/article/10.1007%2Fs11626-019-00403-x https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6881255/ Morera E, Steinhäuser SS, Budkova Z, Ingthorsson S, Kricker J, Krueger A, Traustadottir GA, Gudjonsson T. YKL-40/CHI3L1 facilitates migration and invasion in HER2 overexpressing breast epithelial progenitor cells and generates a niche for capillary-like network formation. In Vitro Cell Dev Biol Anim. 2019 Dec;55(10):838-853. doi:10.1007/s11626-019-00403-x. 31482369 doi:10.1007/s11626-019-00403-x http://hdl.handle.net/2336/621252 1543-706X In vitro cellular & developmental biology. Animal Open Access - Opinn aðgangur In vitro cellular & developmental biology. Animal 55 10 838 853 Germany Angiogenesis Epithelial to mesenchymal transition (EMT) Invasive breast cancer Migration YKL-40/CHI3L1 Brjóstakrabbamein Neoplastic Stem Cells Article 2019 ftlandspitaliuni https://doi.org/10.1007/s11626-019-00403-x 2022-05-29T08:22:29Z To access publisher's full text version of this article, please click on the hyperlink in Additional Links field or click on the hyperlink at the top of the page marked Download Epithelial to mesenchymal transition (EMT) is a developmental event that is hijacked in some diseases such as fibrosis and cancer. In cancer, EMT has been linked to increased invasion and metastasis and is generally associated with a poor prognosis. In this study, we have compared phenotypic and functional differences between two isogenic cell lines with an EMT profile: D492M and D492HER2 that are both derived from D492, a breast epithelial cell line with stem cell properties. D492M is non-tumorigenic while D492HER2 is tumorigenic. Thus, the aim of this study was to analyze the expression profile of these cell lines, identify potential oncogenes, and evaluate their effects on cellular phenotype. We performed transcriptome and secretome analyses of D492M and D492HER2 and verified expression of selected genes at the RNA and protein level. One candidate, YKL-40 (also known as CHI3L1), was selected for further studies due to its differential expression between D492M and D492HER2, being considerably higher in D492HER2. YKL-40 has been linked to chronic inflammation diseases and cancer, yet its function is not fully understood. Knock-down experiments of YKL-40 in D492HER2 resulted in reduced migration and invasion as well as reduced ability to induce angiogenesis in an in vitro assay, plus changes in the EMT-phenotype. In summary, our data suggest that YKL-40 may provide D492HER2 with increased aggressiveness, supporting cancer progression and facilitating angiogenesis. University of Iceland Research fund Landspitali Haskolasjukrahus Science fund Gongum saman supporting group for breast cancer research in Iceland Grant of Excellence, Icelandic Science and Technology Policy Article in Journal/Newspaper Iceland Hirsla - Landspítali University Hospital research archive In Vitro Cellular & Developmental Biology - Animal 55 10 838 853 |
institution |
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collection |
Hirsla - Landspítali University Hospital research archive |
op_collection_id |
ftlandspitaliuni |
language |
English |
topic |
Angiogenesis Epithelial to mesenchymal transition (EMT) Invasive breast cancer Migration YKL-40/CHI3L1 Brjóstakrabbamein Neoplastic Stem Cells |
spellingShingle |
Angiogenesis Epithelial to mesenchymal transition (EMT) Invasive breast cancer Migration YKL-40/CHI3L1 Brjóstakrabbamein Neoplastic Stem Cells Morera, Erika Steinhäuser, Sarah Sophie Budkova, Zuzana Ingthorsson, Saevar Kricker, Jennifer Krueger, Aileen Traustadottir, Gunnhildur Asta Gudjonsson, Thorarinn YKL-40/CHI3L1 facilitates migration and invasion in HER2 overexpressing breast epithelial progenitor cells and generates a niche for capillary-like network formation. |
topic_facet |
Angiogenesis Epithelial to mesenchymal transition (EMT) Invasive breast cancer Migration YKL-40/CHI3L1 Brjóstakrabbamein Neoplastic Stem Cells |
description |
To access publisher's full text version of this article, please click on the hyperlink in Additional Links field or click on the hyperlink at the top of the page marked Download Epithelial to mesenchymal transition (EMT) is a developmental event that is hijacked in some diseases such as fibrosis and cancer. In cancer, EMT has been linked to increased invasion and metastasis and is generally associated with a poor prognosis. In this study, we have compared phenotypic and functional differences between two isogenic cell lines with an EMT profile: D492M and D492HER2 that are both derived from D492, a breast epithelial cell line with stem cell properties. D492M is non-tumorigenic while D492HER2 is tumorigenic. Thus, the aim of this study was to analyze the expression profile of these cell lines, identify potential oncogenes, and evaluate their effects on cellular phenotype. We performed transcriptome and secretome analyses of D492M and D492HER2 and verified expression of selected genes at the RNA and protein level. One candidate, YKL-40 (also known as CHI3L1), was selected for further studies due to its differential expression between D492M and D492HER2, being considerably higher in D492HER2. YKL-40 has been linked to chronic inflammation diseases and cancer, yet its function is not fully understood. Knock-down experiments of YKL-40 in D492HER2 resulted in reduced migration and invasion as well as reduced ability to induce angiogenesis in an in vitro assay, plus changes in the EMT-phenotype. In summary, our data suggest that YKL-40 may provide D492HER2 with increased aggressiveness, supporting cancer progression and facilitating angiogenesis. University of Iceland Research fund Landspitali Haskolasjukrahus Science fund Gongum saman supporting group for breast cancer research in Iceland Grant of Excellence, Icelandic Science and Technology Policy |
author2 |
1 Stem Cell Research Unit, Biomedical Center, Department of Anatomy, Faculty of Medicine, School of Health Sciences, University of Iceland, Vatnsmyrarvegi 16, 101, Reykjavik, Iceland. 2 Heidelberg Institute for Stem Cell Technology and Experimental Medicine, Heidelberg, Germany. 3 Stem Cell Research Unit, Biomedical Center, Department of Anatomy, Faculty of Medicine, School of Health Sciences, University of Iceland, Vatnsmyrarvegi 16, 101, Reykjavik, Iceland. tgudjons@hi.is. 4 Department of Laboratory Hematology, Landspitali - University Hospital, Reykjavik, Iceland. tgudjons@hi.is. |
format |
Article in Journal/Newspaper |
author |
Morera, Erika Steinhäuser, Sarah Sophie Budkova, Zuzana Ingthorsson, Saevar Kricker, Jennifer Krueger, Aileen Traustadottir, Gunnhildur Asta Gudjonsson, Thorarinn |
author_facet |
Morera, Erika Steinhäuser, Sarah Sophie Budkova, Zuzana Ingthorsson, Saevar Kricker, Jennifer Krueger, Aileen Traustadottir, Gunnhildur Asta Gudjonsson, Thorarinn |
author_sort |
Morera, Erika |
title |
YKL-40/CHI3L1 facilitates migration and invasion in HER2 overexpressing breast epithelial progenitor cells and generates a niche for capillary-like network formation. |
title_short |
YKL-40/CHI3L1 facilitates migration and invasion in HER2 overexpressing breast epithelial progenitor cells and generates a niche for capillary-like network formation. |
title_full |
YKL-40/CHI3L1 facilitates migration and invasion in HER2 overexpressing breast epithelial progenitor cells and generates a niche for capillary-like network formation. |
title_fullStr |
YKL-40/CHI3L1 facilitates migration and invasion in HER2 overexpressing breast epithelial progenitor cells and generates a niche for capillary-like network formation. |
title_full_unstemmed |
YKL-40/CHI3L1 facilitates migration and invasion in HER2 overexpressing breast epithelial progenitor cells and generates a niche for capillary-like network formation. |
title_sort |
ykl-40/chi3l1 facilitates migration and invasion in her2 overexpressing breast epithelial progenitor cells and generates a niche for capillary-like network formation. |
publisher |
Springer |
publishDate |
2019 |
url |
http://hdl.handle.net/2336/621252 https://doi.org/10.1007/s11626-019-00403-x |
genre |
Iceland |
genre_facet |
Iceland |
op_source |
In vitro cellular & developmental biology. Animal 55 10 838 853 Germany |
op_relation |
https://link.springer.com/article/10.1007%2Fs11626-019-00403-x https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6881255/ Morera E, Steinhäuser SS, Budkova Z, Ingthorsson S, Kricker J, Krueger A, Traustadottir GA, Gudjonsson T. YKL-40/CHI3L1 facilitates migration and invasion in HER2 overexpressing breast epithelial progenitor cells and generates a niche for capillary-like network formation. In Vitro Cell Dev Biol Anim. 2019 Dec;55(10):838-853. doi:10.1007/s11626-019-00403-x. 31482369 doi:10.1007/s11626-019-00403-x http://hdl.handle.net/2336/621252 1543-706X In vitro cellular & developmental biology. Animal |
op_rights |
Open Access - Opinn aðgangur |
op_doi |
https://doi.org/10.1007/s11626-019-00403-x |
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In Vitro Cellular & Developmental Biology - Animal |
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55 |
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10 |
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