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Novel mechanism for OSM-promoted extracellular matrix remodeling in breast cancer: LOXL2 upregulation and subsequent ECM alignment
Invasive ductal carcinoma (IDC) is a serious problem for patients as it metastasizes, decreasing 5-year patient survival from > 95 to ~ 27%. The breast tumor microenvironment (TME) is often saturated with proinflammatory cytokines, such as oncostatin M (OSM), which promote epithelial-to-mesenchym...
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Published in: | Breast cancer research : BCR 2021-05, Vol.23 (1), p.56-56, Article 56 |
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description | Invasive ductal carcinoma (IDC) is a serious problem for patients as it metastasizes, decreasing 5-year patient survival from > 95 to ~ 27%. The breast tumor microenvironment (TME) is often saturated with proinflammatory cytokines, such as oncostatin M (OSM), which promote epithelial-to-mesenchymal transitions (EMT) in IDC and increased metastasis. The extracellular matrix (ECM) also plays an important role in promoting invasive and metastatic potential of IDC. Specifically, the reorganization and alignment of collagen fibers in stromal ECM leads to directed tumor cell motility, which promotes metastasis. Lysyl oxidase like-2 (LOXL2) catalyzes ECM remodeling by crosslinking of collagen I in the ECM. We propose a novel mechanism whereby OSM induces LOXL2 expression, mediating stromal ECM remodeling of the breast TME.
Bioinformatics was utilized to determine survival and gene correlation in patients. IDC cell lines were treated with OSM (also IL-6, LIF, and IL-1β) and analyzed for LOXL2 expression by qRT-PCR and immunolabelling techniques. Collagen I contraction assays, 3D invasion assays, and confocal microscopy were performed with and without LOXL2 inhibition to determine the impact of OSM-induced LOXL2 on the ECM.
Our studies demonstrate that IDC patients with high LOXL2 and OSM co-expression had worse rates of metastasis-free survival than those with high levels of either, individually, and LOXL2 expression is positively correlated to OSM/OSM receptor (OSMR) expression in IDC patients. Furthermore, human IDC cells treated with OSM resulted in a significant increase in LOXL2 mRNA, which led to upregulated protein expression of secreted, glycosylated, and enzymatically active LOXL2. The expression of LOXL2 in IDC cells did not affect OSM-promoted EMT, and LOXL2 was localized to the cytoplasm and/or secreted. OSM-induced LOXL2 promoted an increase in ECM collagen I fiber crosslinking, which led to significant fiber alignment between cells and increased IDC cell invasion.
Aligned collagen fibers in the ECM provide pathways for tumor cells to migrate more easily through the stroma to nearby vasculature and tissue. These results provide a new paradigm through which proinflammatory cytokine OSM promotes tumor progression. Understanding the nuances in IDC metastasis will lead to better potential therapeutics to combat against the possibility. |
doi_str_mv | 10.1186/s13058-021-01430-x |
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Bioinformatics was utilized to determine survival and gene correlation in patients. IDC cell lines were treated with OSM (also IL-6, LIF, and IL-1β) and analyzed for LOXL2 expression by qRT-PCR and immunolabelling techniques. Collagen I contraction assays, 3D invasion assays, and confocal microscopy were performed with and without LOXL2 inhibition to determine the impact of OSM-induced LOXL2 on the ECM.
Our studies demonstrate that IDC patients with high LOXL2 and OSM co-expression had worse rates of metastasis-free survival than those with high levels of either, individually, and LOXL2 expression is positively correlated to OSM/OSM receptor (OSMR) expression in IDC patients. Furthermore, human IDC cells treated with OSM resulted in a significant increase in LOXL2 mRNA, which led to upregulated protein expression of secreted, glycosylated, and enzymatically active LOXL2. The expression of LOXL2 in IDC cells did not affect OSM-promoted EMT, and LOXL2 was localized to the cytoplasm and/or secreted. OSM-induced LOXL2 promoted an increase in ECM collagen I fiber crosslinking, which led to significant fiber alignment between cells and increased IDC cell invasion.
Aligned collagen fibers in the ECM provide pathways for tumor cells to migrate more easily through the stroma to nearby vasculature and tissue. These results provide a new paradigm through which proinflammatory cytokine OSM promotes tumor progression. Understanding the nuances in IDC metastasis will lead to better potential therapeutics to combat against the possibility.</description><identifier>ISSN: 1465-542X</identifier><identifier>ISSN: 1465-5411</identifier><identifier>EISSN: 1465-542X</identifier><identifier>DOI: 10.1186/s13058-021-01430-x</identifier><identifier>PMID: 34011405</identifier><language>eng</language><publisher>England: BioMed Central Ltd</publisher><subject>Amino Acid Oxidoreductases - genetics ; Amino Acid Oxidoreductases - metabolism ; Analysis ; Bioinformatics ; Breast cancer ; Breast Neoplasms - genetics ; Breast Neoplasms - metabolism ; Breast Neoplasms - pathology ; Carcinoma, Ductal, Breast - genetics ; Carcinoma, Ductal, Breast - metabolism ; Carcinoma, Ductal, Breast - pathology ; Cell Line, Tumor ; Cell migration ; Collagen ; Collagen (type I) ; Collagen Type I - metabolism ; Confocal microscopy ; Contraction ; Crosslinked polymers ; Cytokines ; Cytoplasm ; Development and progression ; Enzymes ; Epithelial-Mesenchymal Transition - genetics ; Extracellular matrix ; Extracellular Matrix - metabolism ; Female ; Fibers ; Gene expression ; Glycosylation ; Humans ; IL-1β ; Inflammation ; Interleukin 6 ; Invasiveness ; LOXL2 ; Lysyl oxidase ; Medical prognosis ; Medical research ; Medicine, Experimental ; Mesenchyme ; Metastases ; Metastasis ; Motility ; mRNA ; Neoplasm Metastasis ; Oncostatin M ; Oncostatin M - genetics ; Oncostatin M - metabolism ; Oncostatin M - pharmacology ; Oncostatin M Receptor beta Subunit - genetics ; Oncostatin M Receptor beta Subunit - metabolism ; OSM ; Oxidases ; Patients ; Prognosis ; Proteins ; Signal Transduction ; Stroma ; Tumor cells ; Tumor Microenvironment ; Up-Regulation - genetics</subject><ispartof>Breast cancer research : BCR, 2021-05, Vol.23 (1), p.56-56, Article 56</ispartof><rights>COPYRIGHT 2021 BioMed Central Ltd.</rights><rights>2021. This work is licensed 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><rights>The Author(s) 2021</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c563t-6198778ffe03732aa40072a540e17ab962767958e20b78feec825ead1551745d3</citedby><cites>FETCH-LOGICAL-c563t-6198778ffe03732aa40072a540e17ab962767958e20b78feec825ead1551745d3</cites><orcidid>0000-0001-5715-472X</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/PMC8132418/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/2528895941?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,25753,27924,27925,37012,37013,44590,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/34011405$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Dinca, Simion C</creatorcontrib><creatorcontrib>Greiner, Daniel</creatorcontrib><creatorcontrib>Weidenfeld, Keren</creatorcontrib><creatorcontrib>Bond, Laura</creatorcontrib><creatorcontrib>Barkan, Dalit</creatorcontrib><creatorcontrib>Jorcyk, Cheryl L</creatorcontrib><title>Novel mechanism for OSM-promoted extracellular matrix remodeling in breast cancer: LOXL2 upregulation and subsequent ECM alignment</title><title>Breast cancer research : BCR</title><addtitle>Breast Cancer Res</addtitle><description>Invasive ductal carcinoma (IDC) is a serious problem for patients as it metastasizes, decreasing 5-year patient survival from > 95 to ~ 27%. The breast tumor microenvironment (TME) is often saturated with proinflammatory cytokines, such as oncostatin M (OSM), which promote epithelial-to-mesenchymal transitions (EMT) in IDC and increased metastasis. The extracellular matrix (ECM) also plays an important role in promoting invasive and metastatic potential of IDC. Specifically, the reorganization and alignment of collagen fibers in stromal ECM leads to directed tumor cell motility, which promotes metastasis. Lysyl oxidase like-2 (LOXL2) catalyzes ECM remodeling by crosslinking of collagen I in the ECM. We propose a novel mechanism whereby OSM induces LOXL2 expression, mediating stromal ECM remodeling of the breast TME.
Bioinformatics was utilized to determine survival and gene correlation in patients. IDC cell lines were treated with OSM (also IL-6, LIF, and IL-1β) and analyzed for LOXL2 expression by qRT-PCR and immunolabelling techniques. Collagen I contraction assays, 3D invasion assays, and confocal microscopy were performed with and without LOXL2 inhibition to determine the impact of OSM-induced LOXL2 on the ECM.
Our studies demonstrate that IDC patients with high LOXL2 and OSM co-expression had worse rates of metastasis-free survival than those with high levels of either, individually, and LOXL2 expression is positively correlated to OSM/OSM receptor (OSMR) expression in IDC patients. Furthermore, human IDC cells treated with OSM resulted in a significant increase in LOXL2 mRNA, which led to upregulated protein expression of secreted, glycosylated, and enzymatically active LOXL2. The expression of LOXL2 in IDC cells did not affect OSM-promoted EMT, and LOXL2 was localized to the cytoplasm and/or secreted. OSM-induced LOXL2 promoted an increase in ECM collagen I fiber crosslinking, which led to significant fiber alignment between cells and increased IDC cell invasion.
Aligned collagen fibers in the ECM provide pathways for tumor cells to migrate more easily through the stroma to nearby vasculature and tissue. These results provide a new paradigm through which proinflammatory cytokine OSM promotes tumor progression. Understanding the nuances in IDC metastasis will lead to better potential therapeutics to combat against the possibility.</description><subject>Amino Acid Oxidoreductases - genetics</subject><subject>Amino Acid Oxidoreductases - metabolism</subject><subject>Analysis</subject><subject>Bioinformatics</subject><subject>Breast cancer</subject><subject>Breast Neoplasms - genetics</subject><subject>Breast Neoplasms - metabolism</subject><subject>Breast Neoplasms - pathology</subject><subject>Carcinoma, Ductal, Breast - genetics</subject><subject>Carcinoma, Ductal, Breast - metabolism</subject><subject>Carcinoma, Ductal, Breast - pathology</subject><subject>Cell Line, Tumor</subject><subject>Cell migration</subject><subject>Collagen</subject><subject>Collagen (type I)</subject><subject>Collagen Type I - metabolism</subject><subject>Confocal microscopy</subject><subject>Contraction</subject><subject>Crosslinked polymers</subject><subject>Cytokines</subject><subject>Cytoplasm</subject><subject>Development and progression</subject><subject>Enzymes</subject><subject>Epithelial-Mesenchymal Transition - genetics</subject><subject>Extracellular matrix</subject><subject>Extracellular Matrix - metabolism</subject><subject>Female</subject><subject>Fibers</subject><subject>Gene expression</subject><subject>Glycosylation</subject><subject>Humans</subject><subject>IL-1β</subject><subject>Inflammation</subject><subject>Interleukin 6</subject><subject>Invasiveness</subject><subject>LOXL2</subject><subject>Lysyl oxidase</subject><subject>Medical prognosis</subject><subject>Medical research</subject><subject>Medicine, Experimental</subject><subject>Mesenchyme</subject><subject>Metastases</subject><subject>Metastasis</subject><subject>Motility</subject><subject>mRNA</subject><subject>Neoplasm Metastasis</subject><subject>Oncostatin M</subject><subject>Oncostatin M - genetics</subject><subject>Oncostatin M - metabolism</subject><subject>Oncostatin M - pharmacology</subject><subject>Oncostatin M Receptor beta Subunit - genetics</subject><subject>Oncostatin M Receptor beta Subunit - metabolism</subject><subject>OSM</subject><subject>Oxidases</subject><subject>Patients</subject><subject>Prognosis</subject><subject>Proteins</subject><subject>Signal Transduction</subject><subject>Stroma</subject><subject>Tumor cells</subject><subject>Tumor Microenvironment</subject><subject>Up-Regulation - genetics</subject><issn>1465-542X</issn><issn>1465-5411</issn><issn>1465-542X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>PIMPY</sourceid><sourceid>DOA</sourceid><recordid>eNptUk1v1DAUjBCIlsIf4IAsceklxZ-JwwGpWhWotGUPgNSb5dgvW68Se7GTarnyy3G6pXQR8sF-zzNjvfEUxWuCzwiR1btEGBayxJSUmHCGy92T4pjwSpSC0-unj85HxYuUNhiTWgr5vDhiHBPCsTgufn0Jt9CjAcyN9i4NqAsRrb5eldsYhjCCRbAbozbQ91OvIxr0GN0ORRiChd75NXIetRF0GpHR3kB8j5ar6yVF0zbCOnNGFzzS3qI0tQl-TOBHdLG4Qrp3az_k6mXxrNN9glf3-0nx_ePFt8Xncrn6dLk4X5ZGVGwsK9LIupZdB5jVjGrNMa6pFhwDqXXbVLSu6kZIoLjNMAAjqQBtiRCk5sKyk-Jyr2uD3qhtdIOOP1XQTt01QlwrHUdnelCmoZVtaU2Z1dzYptUMiDE1loaC7Jqs9WGvtZ3aAazJY0TdH4ge3nh3o9bhVknCKCcyC5zeC8SQPUmjGlyaXdYewpQUFbRpCKVifuvtP9BNmKLPVs0oKRvRcPIXtdZ5AOe7MH_bLKrOq0pwlnNQZdTZf1B5WRicCR46l_sHBLonmBhSitA9zEiwmlOo9ilUOYXqLoVql0lvHrvzQPkTO_Ybg4zYdw</recordid><startdate>20210519</startdate><enddate>20210519</enddate><creator>Dinca, Simion C</creator><creator>Greiner, Daniel</creator><creator>Weidenfeld, Keren</creator><creator>Bond, Laura</creator><creator>Barkan, Dalit</creator><creator>Jorcyk, Cheryl L</creator><general>BioMed Central Ltd</general><general>BioMed Central</general><general>BMC</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>3V.</scope><scope>7TO</scope><scope>7X7</scope><scope>7XB</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</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>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope><orcidid>https://orcid.org/0000-0001-5715-472X</orcidid></search><sort><creationdate>20210519</creationdate><title>Novel mechanism for OSM-promoted extracellular matrix remodeling in breast cancer: LOXL2 upregulation and subsequent ECM alignment</title><author>Dinca, Simion C ; Greiner, Daniel ; Weidenfeld, Keren ; Bond, Laura ; Barkan, Dalit ; Jorcyk, Cheryl L</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c563t-6198778ffe03732aa40072a540e17ab962767958e20b78feec825ead1551745d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Amino Acid Oxidoreductases - genetics</topic><topic>Amino Acid Oxidoreductases - metabolism</topic><topic>Analysis</topic><topic>Bioinformatics</topic><topic>Breast cancer</topic><topic>Breast Neoplasms - genetics</topic><topic>Breast Neoplasms - metabolism</topic><topic>Breast Neoplasms - pathology</topic><topic>Carcinoma, Ductal, Breast - genetics</topic><topic>Carcinoma, Ductal, Breast - metabolism</topic><topic>Carcinoma, Ductal, Breast - pathology</topic><topic>Cell Line, Tumor</topic><topic>Cell migration</topic><topic>Collagen</topic><topic>Collagen (type I)</topic><topic>Collagen Type I - metabolism</topic><topic>Confocal microscopy</topic><topic>Contraction</topic><topic>Crosslinked polymers</topic><topic>Cytokines</topic><topic>Cytoplasm</topic><topic>Development and progression</topic><topic>Enzymes</topic><topic>Epithelial-Mesenchymal Transition - genetics</topic><topic>Extracellular matrix</topic><topic>Extracellular Matrix - metabolism</topic><topic>Female</topic><topic>Fibers</topic><topic>Gene expression</topic><topic>Glycosylation</topic><topic>Humans</topic><topic>IL-1β</topic><topic>Inflammation</topic><topic>Interleukin 6</topic><topic>Invasiveness</topic><topic>LOXL2</topic><topic>Lysyl oxidase</topic><topic>Medical prognosis</topic><topic>Medical research</topic><topic>Medicine, Experimental</topic><topic>Mesenchyme</topic><topic>Metastases</topic><topic>Metastasis</topic><topic>Motility</topic><topic>mRNA</topic><topic>Neoplasm Metastasis</topic><topic>Oncostatin M</topic><topic>Oncostatin M - genetics</topic><topic>Oncostatin M - metabolism</topic><topic>Oncostatin M - pharmacology</topic><topic>Oncostatin M Receptor beta Subunit - genetics</topic><topic>Oncostatin M Receptor beta Subunit - metabolism</topic><topic>OSM</topic><topic>Oxidases</topic><topic>Patients</topic><topic>Prognosis</topic><topic>Proteins</topic><topic>Signal Transduction</topic><topic>Stroma</topic><topic>Tumor cells</topic><topic>Tumor Microenvironment</topic><topic>Up-Regulation - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Dinca, Simion C</creatorcontrib><creatorcontrib>Greiner, Daniel</creatorcontrib><creatorcontrib>Weidenfeld, Keren</creatorcontrib><creatorcontrib>Bond, Laura</creatorcontrib><creatorcontrib>Barkan, Dalit</creatorcontrib><creatorcontrib>Jorcyk, Cheryl L</creatorcontrib><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>ProQuest Health and Medical</collection><collection>ProQuest Central (purchase pre-March 2016)</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)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>ProQuest Publicly Available Content database</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>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>Breast cancer research : BCR</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Dinca, Simion C</au><au>Greiner, Daniel</au><au>Weidenfeld, Keren</au><au>Bond, Laura</au><au>Barkan, Dalit</au><au>Jorcyk, Cheryl L</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Novel mechanism for OSM-promoted extracellular matrix remodeling in breast cancer: LOXL2 upregulation and subsequent ECM alignment</atitle><jtitle>Breast cancer research : BCR</jtitle><addtitle>Breast Cancer Res</addtitle><date>2021-05-19</date><risdate>2021</risdate><volume>23</volume><issue>1</issue><spage>56</spage><epage>56</epage><pages>56-56</pages><artnum>56</artnum><issn>1465-542X</issn><issn>1465-5411</issn><eissn>1465-542X</eissn><abstract>Invasive ductal carcinoma (IDC) is a serious problem for patients as it metastasizes, decreasing 5-year patient survival from > 95 to ~ 27%. The breast tumor microenvironment (TME) is often saturated with proinflammatory cytokines, such as oncostatin M (OSM), which promote epithelial-to-mesenchymal transitions (EMT) in IDC and increased metastasis. The extracellular matrix (ECM) also plays an important role in promoting invasive and metastatic potential of IDC. Specifically, the reorganization and alignment of collagen fibers in stromal ECM leads to directed tumor cell motility, which promotes metastasis. Lysyl oxidase like-2 (LOXL2) catalyzes ECM remodeling by crosslinking of collagen I in the ECM. We propose a novel mechanism whereby OSM induces LOXL2 expression, mediating stromal ECM remodeling of the breast TME.
Bioinformatics was utilized to determine survival and gene correlation in patients. IDC cell lines were treated with OSM (also IL-6, LIF, and IL-1β) and analyzed for LOXL2 expression by qRT-PCR and immunolabelling techniques. Collagen I contraction assays, 3D invasion assays, and confocal microscopy were performed with and without LOXL2 inhibition to determine the impact of OSM-induced LOXL2 on the ECM.
Our studies demonstrate that IDC patients with high LOXL2 and OSM co-expression had worse rates of metastasis-free survival than those with high levels of either, individually, and LOXL2 expression is positively correlated to OSM/OSM receptor (OSMR) expression in IDC patients. Furthermore, human IDC cells treated with OSM resulted in a significant increase in LOXL2 mRNA, which led to upregulated protein expression of secreted, glycosylated, and enzymatically active LOXL2. The expression of LOXL2 in IDC cells did not affect OSM-promoted EMT, and LOXL2 was localized to the cytoplasm and/or secreted. OSM-induced LOXL2 promoted an increase in ECM collagen I fiber crosslinking, which led to significant fiber alignment between cells and increased IDC cell invasion.
Aligned collagen fibers in the ECM provide pathways for tumor cells to migrate more easily through the stroma to nearby vasculature and tissue. These results provide a new paradigm through which proinflammatory cytokine OSM promotes tumor progression. Understanding the nuances in IDC metastasis will lead to better potential therapeutics to combat against the possibility.</abstract><cop>England</cop><pub>BioMed Central Ltd</pub><pmid>34011405</pmid><doi>10.1186/s13058-021-01430-x</doi><tpages>1</tpages><orcidid>https://orcid.org/0000-0001-5715-472X</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | Amino Acid Oxidoreductases - genetics Amino Acid Oxidoreductases - metabolism Analysis Bioinformatics Breast cancer Breast Neoplasms - genetics Breast Neoplasms - metabolism Breast Neoplasms - pathology Carcinoma, Ductal, Breast - genetics Carcinoma, Ductal, Breast - metabolism Carcinoma, Ductal, Breast - pathology Cell Line, Tumor Cell migration Collagen Collagen (type I) Collagen Type I - metabolism Confocal microscopy Contraction Crosslinked polymers Cytokines Cytoplasm Development and progression Enzymes Epithelial-Mesenchymal Transition - genetics Extracellular matrix Extracellular Matrix - metabolism Female Fibers Gene expression Glycosylation Humans IL-1β Inflammation Interleukin 6 Invasiveness LOXL2 Lysyl oxidase Medical prognosis Medical research Medicine, Experimental Mesenchyme Metastases Metastasis Motility mRNA Neoplasm Metastasis Oncostatin M Oncostatin M - genetics Oncostatin M - metabolism Oncostatin M - pharmacology Oncostatin M Receptor beta Subunit - genetics Oncostatin M Receptor beta Subunit - metabolism OSM Oxidases Patients Prognosis Proteins Signal Transduction Stroma Tumor cells Tumor Microenvironment Up-Regulation - genetics |
title | Novel mechanism for OSM-promoted extracellular matrix remodeling in breast cancer: LOXL2 upregulation and subsequent ECM alignment |
url | http://sfxeu10.hosted.exlibrisgroup.com/loughborough?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-24T16%3A52%3A50IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_doaj_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Novel%20mechanism%20for%20OSM-promoted%20extracellular%20matrix%20remodeling%20in%20breast%20cancer:%20LOXL2%20upregulation%20and%20subsequent%20ECM%20alignment&rft.jtitle=Breast%20cancer%20research%20:%20BCR&rft.au=Dinca,%20Simion%20C&rft.date=2021-05-19&rft.volume=23&rft.issue=1&rft.spage=56&rft.epage=56&rft.pages=56-56&rft.artnum=56&rft.issn=1465-542X&rft.eissn=1465-542X&rft_id=info:doi/10.1186/s13058-021-01430-x&rft_dat=%3Cgale_doaj_%3EA665435426%3C/gale_doaj_%3E%3Cgrp_id%3Ecdi_FETCH-LOGICAL-c563t-6198778ffe03732aa40072a540e17ab962767958e20b78feec825ead1551745d3%3C/grp_id%3E%3Coa%3E%3C/oa%3E%3Curl%3E%3C/url%3E&rft_id=info:oai/&rft_pqid=2528895941&rft_id=info:pmid/34011405&rft_galeid=A665435426&rfr_iscdi=true |