We are analyzing https://link.springer.com/article/10.1186/s12964-017-0212-z.

Title:
Frequent overexpression of AMAP1, an Arf6 effector in cell invasion, is characteristic of the MMTV-PyMT rather than the MMTV-Neu human breast cancer model | Cell Communication and Signaling
Description:
Background The small GTPase Arf6 and its downstream effector AMAP1 (also called ASAP1/DDEF1) constitute a signaling pathway promoting cell invasion, in which AMAP1 interacts with several different proteins, including PRKD2, EPB41L5, paxillin, and cortactin. Components of this pathway are often overexpressed in human breast cancer cells, to be correlated with poor prognosis of the patients, whereas overexpression of the Arf6 pathway did not correlate with the four main molecular classes of human breast tumors. In this pathway, receptor tyrosine kinases, including EGFR and Her2, activate Arf6 via GEP100. MMTV-PyMT mice and MMTV-Neu mice are well-established models of human breast cancer, and exhibit the early dissemination and the lung metastasis, by utilizing protein tyrosine phosphorylation for oncogenesis. PyMT-tumors and Neu-tumors are known to have overlapping gene expression profiles, which primarily correspond to the luminal B-type of human mammary tumors, although they differ in the time necessary for tumor onset and metastasis. Given the common usage of protein tyrosine phosphorylation, as well as the frequent use of these animal models for studying breast cancer at the molecular level, we here investigated whether mammary tumors in these mouse models utilize the Arf6-based pathway for invasion. Methods Expression levels of Arf6, AMAP1, and GEP100 were analyzed in PyMT-tumors and Neu-tumors by western blotting. Expression of Arf6 and AMAP1 was also analyzed by immunohistochemistry. The involvement of AMAP1 in invasion, and the possible correlation of its high expression levels with cancer mesenchymal properties were also investigated. Results We found that PyMT-tumors, but not Neu-tumors, frequently overexpress AMAP1 and use it for invasion, whereas both types of tumors expressed Arf6 and GEP100 at different levels. High levels of the AMAP1 expression among PyMT-tumor cells were frequently correlated with loss of the epithelial marker CK8 and also with expression of the mesenchymal marker vimentin both at the primary sites and at sites of the lung metastases. Conclusions PyMT-tumors appear to frequently utilize the Arf6-based invasive machinery, whereas Neu-tumors do not. Our results suggest that MMTV-PyMT mice, rather than MMTV-Neu mice, are useful to study the Arf6-based mammary tumor malignancies, as a representative model of human breast cancer.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {📚}

Science
Education
Health & Fitness

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 5,000,019 visitors per month in the current month.
However, some sources were not loaded, we suggest to reload the page to get complete results.

check SE Ranking
check Ahrefs
check Similarweb
check Ubersuggest
check Semrush

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

We're unsure if the website is profiting.

Earning money isn't the goal of every website; some are designed to offer support or promote social causes. People have different reasons for creating websites. This might be one such reason. Link.springer.com might be plotting its profit, but the way they're doing it isn't detectable yet.

Keywords {🔍}

cancer, cells, amap, breast, pubmed, article, arf, mice, google, scholar, tumor, cell, expression, cas, hashimoto, invasion, pathway, levels, tumors, fig, mouse, human, performed, mmtvpymt, primary, central, mmtvneu, metastasis, pymt, model, pymttumors, arfbased, high, analysis, protein, mammary, weeks, sabe, antibodies, models, mrna, data, gep, animal, previously, receptor, neutumors, frequently, vimentin, sites,

Topics {✒️}

semi-quantitative rt-pcr analysis guanine nucleotide-exchanging factor primary mammary stem article download pdf confocal laser-scanning microscope post-transcriptionally regulate cadherin live-cell imaging analysis metastatic breast cancers cancer-specific metabolic rewiring pathway downregulates e-cadherin tumour-initiating cells egf-induced cancer invasion pymt-induced breast cancer mmtv-neu mice start mmtv-pymt mice start arf6-based invasive machinery mmtv-pymt mouse model peroxidase-conjugated donkey antibodies drives arf6-based invasion full size image arf6-based pathway appears mmtv-neu tumor cells mmtv-pymt mice provide mmtv-pymt tumor cells live-cell imaging shrna-mediated gene silencing alexa488-conjugated goat antibodies cy3-conjugated donkey antibodies luminal b-type breast conservative therapy ires-mediated translational control human breast cancer receptor tyrosine kinases full access pymt-tumor cells demonstrate privacy choices/manage cookies animal model system breast cancer malignancy nat rev cancer breast cancer res related subjects 27-hydroxycholesterol links hypercholesterolemia metastatic breast cancer focal adhesion dynamics human mammary tumors breast cancer invasion studying breast cancer breast cancer subgroups breast cancer pathophysiology mmtv-neu mice

Schema {🗺️}

WebPage:
      mainEntity:
         headline:Frequent overexpression of AMAP1, an Arf6 effector in cell invasion, is characteristic of the MMTV-PyMT rather than the MMTV-Neu human breast cancer model
         description:The small GTPase Arf6 and its downstream effector AMAP1 (also called ASAP1/DDEF1) constitute a signaling pathway promoting cell invasion, in which AMAP1 interacts with several different proteins, including PRKD2, EPB41L5, paxillin, and cortactin. Components of this pathway are often overexpressed in human breast cancer cells, to be correlated with poor prognosis of the patients, whereas overexpression of the Arf6 pathway did not correlate with the four main molecular classes of human breast tumors. In this pathway, receptor tyrosine kinases, including EGFR and Her2, activate Arf6 via GEP100. MMTV-PyMT mice and MMTV-Neu mice are well-established models of human breast cancer, and exhibit the early dissemination and the lung metastasis, by utilizing protein tyrosine phosphorylation for oncogenesis. PyMT-tumors and Neu-tumors are known to have overlapping gene expression profiles, which primarily correspond to the luminal B-type of human mammary tumors, although they differ in the time necessary for tumor onset and metastasis. Given the common usage of protein tyrosine phosphorylation, as well as the frequent use of these animal models for studying breast cancer at the molecular level, we here investigated whether mammary tumors in these mouse models utilize the Arf6-based pathway for invasion. Expression levels of Arf6, AMAP1, and GEP100 were analyzed in PyMT-tumors and Neu-tumors by western blotting. Expression of Arf6 and AMAP1 was also analyzed by immunohistochemistry. The involvement of AMAP1 in invasion, and the possible correlation of its high expression levels with cancer mesenchymal properties were also investigated. We found that PyMT-tumors, but not Neu-tumors, frequently overexpress AMAP1 and use it for invasion, whereas both types of tumors expressed Arf6 and GEP100 at different levels. High levels of the AMAP1 expression among PyMT-tumor cells were frequently correlated with loss of the epithelial marker CK8 and also with expression of the mesenchymal marker vimentin both at the primary sites and at sites of the lung metastases. PyMT-tumors appear to frequently utilize the Arf6-based invasive machinery, whereas Neu-tumors do not. Our results suggest that MMTV-PyMT mice, rather than MMTV-Neu mice, are useful to study the Arf6-based mammary tumor malignancies, as a representative model of human breast cancer.
         datePublished:2018-01-05T00:00:00Z
         dateModified:2018-01-05T00:00:00Z
         pageStart:1
         pageEnd:9
         license:http://creativecommons.org/publicdomain/zero/1.0/
         sameAs:https://doi.org/10.1186/s12964-017-0212-z
         keywords:
            MMTV-PyMT mice
            MMTV-Neu mice
            Luminal B-type of human breast cancer
            The Arf6-based pathway
            AMAP1
            Cell Biology
            Protein-Ligand Interactions
            Receptors
            Cytokines and Growth Factors
         image:
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1186%2Fs12964-017-0212-z/MediaObjects/12964_2017_212_Fig1_HTML.gif
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1186%2Fs12964-017-0212-z/MediaObjects/12964_2017_212_Fig2_HTML.gif
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1186%2Fs12964-017-0212-z/MediaObjects/12964_2017_212_Fig3_HTML.gif
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1186%2Fs12964-017-0212-z/MediaObjects/12964_2017_212_Fig4_HTML.gif
         isPartOf:
            name:Cell Communication and Signaling
            issn:
               1478-811X
            volumeNumber:16
            type:
               Periodical
               PublicationVolume
         publisher:
            name:BioMed Central
            logo:
               url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
               type:ImageObject
            type:Organization
         author:
               name:Yutaro Otsuka
               affiliation:
                     name:Hokkaido University
                     address:
                        name:Department of Molecular Biology, Graduate School of Medicine, Hokkaido University, Sapporo, Japan
                        type:PostalAddress
                     type:Organization
               type:Person
               name:Tsukasa Oikawa
               affiliation:
                     name:Hokkaido University
                     address:
                        name:Department of Molecular Biology, Graduate School of Medicine, Hokkaido University, Sapporo, Japan
                        type:PostalAddress
                     type:Organization
               email:[email protected]
               type:Person
               name:Hinako Yoshino
               affiliation:
                     name:Hokkaido University
                     address:
                        name:Department of Molecular Biology, Graduate School of Medicine, Hokkaido University, Sapporo, Japan
                        type:PostalAddress
                     type:Organization
               type:Person
               name:Shigeru Hashimoto
               affiliation:
                     name:Hokkaido University
                     address:
                        name:Department of Molecular Biology, Graduate School of Medicine, Hokkaido University, Sapporo, Japan
                        type:PostalAddress
                     type:Organization
               type:Person
               name:Haruka Handa
               affiliation:
                     name:Hokkaido University
                     address:
                        name:Department of Molecular Biology, Graduate School of Medicine, Hokkaido University, Sapporo, Japan
                        type:PostalAddress
                     type:Organization
               type:Person
               name:Hiroki Yamamoto
               affiliation:
                     name:Hokkaido University
                     address:
                        name:Department of Molecular Biology, Graduate School of Medicine, Hokkaido University, Sapporo, Japan
                        type:PostalAddress
                     type:Organization
               type:Person
               name:Ari Hashimoto
               affiliation:
                     name:Hokkaido University
                     address:
                        name:Department of Molecular Biology, Graduate School of Medicine, Hokkaido University, Sapporo, Japan
                        type:PostalAddress
                     type:Organization
               type:Person
               name:Hisataka Sabe
               affiliation:
                     name:Hokkaido University
                     address:
                        name:Department of Molecular Biology, Graduate School of Medicine, Hokkaido University, Sapporo, Japan
                        type:PostalAddress
                     type:Organization
               email:[email protected]
               type:Person
         isAccessibleForFree:1
         type:ScholarlyArticle
      context:https://schema.org
ScholarlyArticle:
      headline:Frequent overexpression of AMAP1, an Arf6 effector in cell invasion, is characteristic of the MMTV-PyMT rather than the MMTV-Neu human breast cancer model
      description:The small GTPase Arf6 and its downstream effector AMAP1 (also called ASAP1/DDEF1) constitute a signaling pathway promoting cell invasion, in which AMAP1 interacts with several different proteins, including PRKD2, EPB41L5, paxillin, and cortactin. Components of this pathway are often overexpressed in human breast cancer cells, to be correlated with poor prognosis of the patients, whereas overexpression of the Arf6 pathway did not correlate with the four main molecular classes of human breast tumors. In this pathway, receptor tyrosine kinases, including EGFR and Her2, activate Arf6 via GEP100. MMTV-PyMT mice and MMTV-Neu mice are well-established models of human breast cancer, and exhibit the early dissemination and the lung metastasis, by utilizing protein tyrosine phosphorylation for oncogenesis. PyMT-tumors and Neu-tumors are known to have overlapping gene expression profiles, which primarily correspond to the luminal B-type of human mammary tumors, although they differ in the time necessary for tumor onset and metastasis. Given the common usage of protein tyrosine phosphorylation, as well as the frequent use of these animal models for studying breast cancer at the molecular level, we here investigated whether mammary tumors in these mouse models utilize the Arf6-based pathway for invasion. Expression levels of Arf6, AMAP1, and GEP100 were analyzed in PyMT-tumors and Neu-tumors by western blotting. Expression of Arf6 and AMAP1 was also analyzed by immunohistochemistry. The involvement of AMAP1 in invasion, and the possible correlation of its high expression levels with cancer mesenchymal properties were also investigated. We found that PyMT-tumors, but not Neu-tumors, frequently overexpress AMAP1 and use it for invasion, whereas both types of tumors expressed Arf6 and GEP100 at different levels. High levels of the AMAP1 expression among PyMT-tumor cells were frequently correlated with loss of the epithelial marker CK8 and also with expression of the mesenchymal marker vimentin both at the primary sites and at sites of the lung metastases. PyMT-tumors appear to frequently utilize the Arf6-based invasive machinery, whereas Neu-tumors do not. Our results suggest that MMTV-PyMT mice, rather than MMTV-Neu mice, are useful to study the Arf6-based mammary tumor malignancies, as a representative model of human breast cancer.
      datePublished:2018-01-05T00:00:00Z
      dateModified:2018-01-05T00:00:00Z
      pageStart:1
      pageEnd:9
      license:http://creativecommons.org/publicdomain/zero/1.0/
      sameAs:https://doi.org/10.1186/s12964-017-0212-z
      keywords:
         MMTV-PyMT mice
         MMTV-Neu mice
         Luminal B-type of human breast cancer
         The Arf6-based pathway
         AMAP1
         Cell Biology
         Protein-Ligand Interactions
         Receptors
         Cytokines and Growth Factors
      image:
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1186%2Fs12964-017-0212-z/MediaObjects/12964_2017_212_Fig1_HTML.gif
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1186%2Fs12964-017-0212-z/MediaObjects/12964_2017_212_Fig2_HTML.gif
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1186%2Fs12964-017-0212-z/MediaObjects/12964_2017_212_Fig3_HTML.gif
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1186%2Fs12964-017-0212-z/MediaObjects/12964_2017_212_Fig4_HTML.gif
      isPartOf:
         name:Cell Communication and Signaling
         issn:
            1478-811X
         volumeNumber:16
         type:
            Periodical
            PublicationVolume
      publisher:
         name:BioMed Central
         logo:
            url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
            type:ImageObject
         type:Organization
      author:
            name:Yutaro Otsuka
            affiliation:
                  name:Hokkaido University
                  address:
                     name:Department of Molecular Biology, Graduate School of Medicine, Hokkaido University, Sapporo, Japan
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Tsukasa Oikawa
            affiliation:
                  name:Hokkaido University
                  address:
                     name:Department of Molecular Biology, Graduate School of Medicine, Hokkaido University, Sapporo, Japan
                     type:PostalAddress
                  type:Organization
            email:[email protected]
            type:Person
            name:Hinako Yoshino
            affiliation:
                  name:Hokkaido University
                  address:
                     name:Department of Molecular Biology, Graduate School of Medicine, Hokkaido University, Sapporo, Japan
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Shigeru Hashimoto
            affiliation:
                  name:Hokkaido University
                  address:
                     name:Department of Molecular Biology, Graduate School of Medicine, Hokkaido University, Sapporo, Japan
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Haruka Handa
            affiliation:
                  name:Hokkaido University
                  address:
                     name:Department of Molecular Biology, Graduate School of Medicine, Hokkaido University, Sapporo, Japan
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Hiroki Yamamoto
            affiliation:
                  name:Hokkaido University
                  address:
                     name:Department of Molecular Biology, Graduate School of Medicine, Hokkaido University, Sapporo, Japan
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Ari Hashimoto
            affiliation:
                  name:Hokkaido University
                  address:
                     name:Department of Molecular Biology, Graduate School of Medicine, Hokkaido University, Sapporo, Japan
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Hisataka Sabe
            affiliation:
                  name:Hokkaido University
                  address:
                     name:Department of Molecular Biology, Graduate School of Medicine, Hokkaido University, Sapporo, Japan
                     type:PostalAddress
                  type:Organization
            email:[email protected]
            type:Person
      isAccessibleForFree:1
["Periodical","PublicationVolume"]:
      name:Cell Communication and Signaling
      issn:
         1478-811X
      volumeNumber:16
Organization:
      name:BioMed Central
      logo:
         url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
         type:ImageObject
      name:Hokkaido University
      address:
         name:Department of Molecular Biology, Graduate School of Medicine, Hokkaido University, Sapporo, Japan
         type:PostalAddress
      name:Hokkaido University
      address:
         name:Department of Molecular Biology, Graduate School of Medicine, Hokkaido University, Sapporo, Japan
         type:PostalAddress
      name:Hokkaido University
      address:
         name:Department of Molecular Biology, Graduate School of Medicine, Hokkaido University, Sapporo, Japan
         type:PostalAddress
      name:Hokkaido University
      address:
         name:Department of Molecular Biology, Graduate School of Medicine, Hokkaido University, Sapporo, Japan
         type:PostalAddress
      name:Hokkaido University
      address:
         name:Department of Molecular Biology, Graduate School of Medicine, Hokkaido University, Sapporo, Japan
         type:PostalAddress
      name:Hokkaido University
      address:
         name:Department of Molecular Biology, Graduate School of Medicine, Hokkaido University, Sapporo, Japan
         type:PostalAddress
      name:Hokkaido University
      address:
         name:Department of Molecular Biology, Graduate School of Medicine, Hokkaido University, Sapporo, Japan
         type:PostalAddress
      name:Hokkaido University
      address:
         name:Department of Molecular Biology, Graduate School of Medicine, Hokkaido University, Sapporo, Japan
         type:PostalAddress
ImageObject:
      url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
Person:
      name:Yutaro Otsuka
      affiliation:
            name:Hokkaido University
            address:
               name:Department of Molecular Biology, Graduate School of Medicine, Hokkaido University, Sapporo, Japan
               type:PostalAddress
            type:Organization
      name:Tsukasa Oikawa
      affiliation:
            name:Hokkaido University
            address:
               name:Department of Molecular Biology, Graduate School of Medicine, Hokkaido University, Sapporo, Japan
               type:PostalAddress
            type:Organization
      email:[email protected]
      name:Hinako Yoshino
      affiliation:
            name:Hokkaido University
            address:
               name:Department of Molecular Biology, Graduate School of Medicine, Hokkaido University, Sapporo, Japan
               type:PostalAddress
            type:Organization
      name:Shigeru Hashimoto
      affiliation:
            name:Hokkaido University
            address:
               name:Department of Molecular Biology, Graduate School of Medicine, Hokkaido University, Sapporo, Japan
               type:PostalAddress
            type:Organization
      name:Haruka Handa
      affiliation:
            name:Hokkaido University
            address:
               name:Department of Molecular Biology, Graduate School of Medicine, Hokkaido University, Sapporo, Japan
               type:PostalAddress
            type:Organization
      name:Hiroki Yamamoto
      affiliation:
            name:Hokkaido University
            address:
               name:Department of Molecular Biology, Graduate School of Medicine, Hokkaido University, Sapporo, Japan
               type:PostalAddress
            type:Organization
      name:Ari Hashimoto
      affiliation:
            name:Hokkaido University
            address:
               name:Department of Molecular Biology, Graduate School of Medicine, Hokkaido University, Sapporo, Japan
               type:PostalAddress
            type:Organization
      name:Hisataka Sabe
      affiliation:
            name:Hokkaido University
            address:
               name:Department of Molecular Biology, Graduate School of Medicine, Hokkaido University, Sapporo, Japan
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Department of Molecular Biology, Graduate School of Medicine, Hokkaido University, Sapporo, Japan
      name:Department of Molecular Biology, Graduate School of Medicine, Hokkaido University, Sapporo, Japan
      name:Department of Molecular Biology, Graduate School of Medicine, Hokkaido University, Sapporo, Japan
      name:Department of Molecular Biology, Graduate School of Medicine, Hokkaido University, Sapporo, Japan
      name:Department of Molecular Biology, Graduate School of Medicine, Hokkaido University, Sapporo, Japan
      name:Department of Molecular Biology, Graduate School of Medicine, Hokkaido University, Sapporo, Japan
      name:Department of Molecular Biology, Graduate School of Medicine, Hokkaido University, Sapporo, Japan
      name:Department of Molecular Biology, Graduate School of Medicine, Hokkaido University, Sapporo, Japan

External Links {🔗}(167)

Analytics and Tracking {📊}

Google Tag Manager

Libraries {📚}

Clipboard.js
Prism.js

CDN Services {📦}

Crossref

5.52s.

LINK . SPRINGER . COM {}