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LINK . SPRINGER . COM {}

  1. Analyzed Page
  2. Matching Content Categories
  3. CMS
  4. Monthly Traffic Estimate
  5. How Does Link.springer.com Make Money
  6. Keywords
  7. Topics
  8. Questions
  9. Schema
  10. External Links
  11. Analytics And Tracking
  12. Libraries
  13. CDN Services

We are analyzing https://link.springer.com/article/10.1007/s00018-009-0089-0.

Title:
Human mesenchymal stem cells induce E-cadherin degradation in breast carcinoma spheroids by activating ADAM10 | Cellular and Molecular Life Sciences
Description:
Mesenchymal stem cells (MSCs) have been shown to communicate with tumor cells. We analyzed the effect of human MSCs (hMSCs) on breast cancer cells in three-dimensional cultures. By using GFP expression and immunohistochemistry, we show that hMSCs invade 3D breast cancer cell aggregates. hMSCs caused breast cancer spheroids to become disorganized which was accompanied by a disruption of cell–cell adhesion, E-cadherin cleavage, and nuclear translocation of E-cadherin, but not by epithelial/mesenchymal transition or by an increase in ERK1/2 activity. In addition, hMSCs enhanced the motility of breast cancer cells. Inhibition of ADAM10 (a disintegrin and metalloprotease 10), known to cleave E-cadherin, prevented both hMSC-mediated E-cadherin cleavage and enhanced migration. Our data suggest that hMSCs interfere with cell–cell adhesion and enhance migration of breast cancer cells by activating ADAM10.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {📚}

  • Science
  • Education
  • Telecommunications

Content Management System {📝}

What CMS is link.springer.com built with?

Custom-built

No common CMS systems were detected on Link.springer.com, and no known web development framework was identified.

Traffic Estimate {📈}

What is the average monthly size of link.springer.com audience?

🌠 Phenomenal Traffic: 5M - 10M visitors per month


Based on our best estimate, this website will receive around 7,642,828 visitors per month in the current month.

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How Does Link.springer.com Make Money? {💸}

We don't see any clear sign of profit-making.

Not all websites are made for profit; some exist to inform or educate users. Or any other reason why people make websites. And this might be the case. Link.springer.com might be cashing in, but we can't detect the method they're using.

Keywords {🔍}

cells, google, scholar, article, cancer, pubmed, cas, mesenchymal, breast, stem, human, cell, ecadherin, dittmer, biol, adam, migration, access, res, chem, privacy, cookies, content, tumor, hmscs, epithelial, mol, doijbcm, data, publish, research, search, spheroids, cellcell, open, marini, sci, halle, information, log, journal, cellular, life, carcinoma, activating, hohlfeld, lĂźtzkendorf, jĂźrgen, adhesion, discover,

Topics {✒️}

epithelial/mesenchymal transition hmsc-mediated e-cadherin cleavage mesenchymal stem cells month download article/chapter mesenchymal stromal cells human bone marrow elevated sdf-1/cxcl12 secretion breast cancer cells breast tumor cells related subjects stem cells 24 fibroblast-led collective invasion breast carcinoma spheroids e-cadherin cleavage full article pdf adam10-mediated release cleaved cytoplasmic domain egf receptor transactivation stromal fibroblasts present cleave e-cadherin generation lentivirus vector high-efficiency transformation e-cadherin fragment e-cadherin molecule mda-mb-231 cells epithelial cells privacy choices/manage cookies protein-coupled receptors solid pseudopapillary tumour cancer cells check access instant access cell–cell adhesion egf induces macropinocytosis vitro propagation consistent features article cellular article dittmer tumor cells cell–cell organization cell migration european economic area e-cadherin conditional packaging system multidrug resistant variant induces luminal repopulation snx1-modulated recycling sustained erk signaling reliable loading control land sachsen-anhalt

Questions {❓}

  • Shchors K, Evan G (2007) Tumor angiogenesis: cause or consequence of cancer?
  • Yen L, Yen M-L (2008) Mesenchymal stem cells and cancer—for better or for worse?

Schema {🗺️}

WebPage:
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         headline:Human mesenchymal stem cells induce E-cadherin degradation in breast carcinoma spheroids by activating ADAM10
         description:Mesenchymal stem cells (MSCs) have been shown to communicate with tumor cells. We analyzed the effect of human MSCs (hMSCs) on breast cancer cells in three-dimensional cultures. By using GFP expression and immunohistochemistry, we show that hMSCs invade 3D breast cancer cell aggregates. hMSCs caused breast cancer spheroids to become disorganized which was accompanied by a disruption of cell–cell adhesion, E-cadherin cleavage, and nuclear translocation of E-cadherin, but not by epithelial/mesenchymal transition or by an increase in ERK1/2 activity. In addition, hMSCs enhanced the motility of breast cancer cells. Inhibition of ADAM10 (a disintegrin and metalloprotease 10), known to cleave E-cadherin, prevented both hMSC-mediated E-cadherin cleavage and enhanced migration. Our data suggest that hMSCs interfere with cell–cell adhesion and enhance migration of breast cancer cells by activating ADAM10.
         datePublished:2009-07-15T00:00:00Z
         dateModified:2009-07-15T00:00:00Z
         pageStart:3053
         pageEnd:3065
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            Spheroids
            Breast cancer
            Migration
            ADAM 10
            E-cadherin
            Cell Biology
            Biomedicine
            general
            Life Sciences
            Biochemistry
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      headline:Human mesenchymal stem cells induce E-cadherin degradation in breast carcinoma spheroids by activating ADAM10
      description:Mesenchymal stem cells (MSCs) have been shown to communicate with tumor cells. We analyzed the effect of human MSCs (hMSCs) on breast cancer cells in three-dimensional cultures. By using GFP expression and immunohistochemistry, we show that hMSCs invade 3D breast cancer cell aggregates. hMSCs caused breast cancer spheroids to become disorganized which was accompanied by a disruption of cell–cell adhesion, E-cadherin cleavage, and nuclear translocation of E-cadherin, but not by epithelial/mesenchymal transition or by an increase in ERK1/2 activity. In addition, hMSCs enhanced the motility of breast cancer cells. Inhibition of ADAM10 (a disintegrin and metalloprotease 10), known to cleave E-cadherin, prevented both hMSC-mediated E-cadherin cleavage and enhanced migration. Our data suggest that hMSCs interfere with cell–cell adhesion and enhance migration of breast cancer cells by activating ADAM10.
      datePublished:2009-07-15T00:00:00Z
      dateModified:2009-07-15T00:00:00Z
      pageStart:3053
      pageEnd:3065
      sameAs:https://doi.org/10.1007/s00018-009-0089-0
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         MSC
         Spheroids
         Breast cancer
         Migration
         ADAM 10
         E-cadherin
         Cell Biology
         Biomedicine
         general
         Life Sciences
         Biochemistry
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            name:Universität Halle
            address:
               name:Zentrum fĂźr Innere Medizin, Klinik fĂźr Innere Medizin IV, Universität Halle, Halle (Saale), Germany
               type:PostalAddress
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            name:Universität Halle
            address:
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      name:Zentrum fĂźr Innere Medizin, Klinik fĂźr Innere Medizin IV, Universität Halle, Halle (Saale), Germany
      name:Zentrum fĂźr Innere Medizin, Klinik fĂźr Innere Medizin IV, Universität Halle, Halle (Saale), Germany
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External Links {🔗}(126)

Analytics and Tracking {📊}

  • Google Tag Manager

Libraries {📚}

  • Clipboard.js
  • Prism.js

CDN Services {📦}

  • Crossref

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