We are analyzing https://link.springer.com/article/10.1186/1471-2407-10-505.

Title:
Changes in cortical cytoskeletal and extracellular matrix gene expression in prostate cancer are related to oncogenic ERG deregulation | BMC Cancer
Description:
Background The cortical cytoskeleton network connects the actin cytoskeleton to various membrane proteins, influencing cell adhesion, polarity, migration and response to extracellular signals. Previous studies have suggested changes in the expression of specific components in prostate cancer, especially of 4.1 proteins (encoded by EPB41 genes) which form nodes in this network. Methods Expression of EPB41L1, EPB41L2, EPB41L3 (protein: 4.1B), EPB41L4B (EHM2), EPB41L5, EPB49 (dematin), VIL2 (ezrin), and DLG1 (summarized as „cortical cytoskeleton" genes) as well as ERG was measured by quantitative RT-PCR in a well-characterized set of 45 M0 prostate adenocarcinoma and 13 benign tissues. Hypermethylation of EPB41L3 and GSTP1 was compared in 93 cancer tissues by methylation-specific PCR. Expression of 4.1B was further studied by immunohistochemistry. Results EPB41L1 and EPB41L3 were significantly downregulated and EPB41L4B was upregulated in cancer tissues. Low EPB41L1 or high EPB41L4B expression were associated with earlier biochemical recurrence. None of the other cortical cytoskeleton genes displayed expression changes, in particular EPB49 and VIL2, despite hints from previous studies. EPB41L3 downregulation was significantly associated with hypermethylation of its promoter and strongly correlated with GSTP1 hypermethylation. Protein 4.1B was detected most strongly in the basal cells of normal prostate epithelia. Its expression in carcinoma cells was similar to the weaker one in normal luminal cells. EPB41L3 downregulation and EPB41L4B upregulation were essentially restricted to the 22 cases with ERG overexpression. Expression changes in EPB41L3 and EPB41L4B closely paralleled those previously observed for the extracellular matrix genes FBLN1 and SPOCK1, respectively. Conclusions Specific changes in the cortical cytoskeleton were observed during prostate cancer progression. They parallel changes in the expression of extracellular matrix components and all together appear to be associated with oncogenic ERG overexpression. We hypothesize that these alterations may contribute to the increased invasivity conferred to prostate cancer cells by ERG deregulation.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {📚}

Education
Health & Fitness
Science

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.

Not all websites focus on profit; some are designed to educate, connect people, or share useful tools. People create websites for numerous reasons. And this could be one such example. Link.springer.com could be getting rich in stealth mode, or the way it's monetizing isn't detectable.

Keywords {🔍}

cancer, expression, prostate, epbl, article, pubmed, erg, cells, cell, google, scholar, genes, protein, hypermethylation, cas, gene, tissues, epblb, cytoskeleton, cortical, benign, proteins, overexpression, dna, gstp, significantly, progression, tissue, glands, epb, cases, tumor, cancers, data, related, carcinoma, methylation, extracellular, schulz, normal, epithelial, prostatic, fig, figure, matrix, ehm, promoter, basal, invasion, family,

Topics {✒️}

guanidinium/acid phenol/chloroform extraction pi3-kinase pathway activation quantitative real-time rt-pcr pre-publication history pre-neoplastic hg-pins glutathione s-transferase pi avidin-biotin-peroxidase reagent article download pdf androgen-regulated fusion partners biotin-conjugated polyvalent antibody full size image lymph-node negative cancers privacy choices/manage cookies erg-low cancer tissues benign prostatic tissue adjacent tissue layers fusion gene placing human discs large numbered tissue samples log-rank test heinrich heine university factor interaction analysis full access high quality dna malignant prostate tissue binds hyaluronic acid rneasy mini kit quantitative rt-pcr carver bs biomed central binding partners comprise finally counter-stained cell cortex connecting stem cell traits extracellular matrix including regulates cell adhesion authors’ original file prostatic intraepithelial neoplasia oncogenic erg deregulation related subjects kaplan-meyer analysis advanced prostate cancer prostate cancer implicates ets gene fusions lymph-node positive cg island methylation extracellular matrix brought cancer-carrying prostates bmc cancer 10 glands stained positive

Schema {🗺️}

WebPage:
      mainEntity:
         headline:Changes in cortical cytoskeletal and extracellular matrix gene expression in prostate cancer are related to oncogenic ERG deregulation
         description:The cortical cytoskeleton network connects the actin cytoskeleton to various membrane proteins, influencing cell adhesion, polarity, migration and response to extracellular signals. Previous studies have suggested changes in the expression of specific components in prostate cancer, especially of 4.1 proteins (encoded by EPB41 genes) which form nodes in this network. Expression of EPB41L1, EPB41L2, EPB41L3 (protein: 4.1B), EPB41L4B (EHM2), EPB41L5, EPB49 (dematin), VIL2 (ezrin), and DLG1 (summarized as „cortical cytoskeleton" genes) as well as ERG was measured by quantitative RT-PCR in a well-characterized set of 45 M0 prostate adenocarcinoma and 13 benign tissues. Hypermethylation of EPB41L3 and GSTP1 was compared in 93 cancer tissues by methylation-specific PCR. Expression of 4.1B was further studied by immunohistochemistry. EPB41L1 and EPB41L3 were significantly downregulated and EPB41L4B was upregulated in cancer tissues. Low EPB41L1 or high EPB41L4B expression were associated with earlier biochemical recurrence. None of the other cortical cytoskeleton genes displayed expression changes, in particular EPB49 and VIL2, despite hints from previous studies. EPB41L3 downregulation was significantly associated with hypermethylation of its promoter and strongly correlated with GSTP1 hypermethylation. Protein 4.1B was detected most strongly in the basal cells of normal prostate epithelia. Its expression in carcinoma cells was similar to the weaker one in normal luminal cells. EPB41L3 downregulation and EPB41L4B upregulation were essentially restricted to the 22 cases with ERG overexpression. Expression changes in EPB41L3 and EPB41L4B closely paralleled those previously observed for the extracellular matrix genes FBLN1 and SPOCK1, respectively. Specific changes in the cortical cytoskeleton were observed during prostate cancer progression. They parallel changes in the expression of extracellular matrix components and all together appear to be associated with oncogenic ERG overexpression. We hypothesize that these alterations may contribute to the increased invasivity conferred to prostate cancer cells by ERG deregulation.
         datePublished:2010-09-22T00:00:00Z
         dateModified:2010-09-22T00:00:00Z
         pageStart:1
         pageEnd:9
         license:http://creativecommons.org/licenses/by/2.0
         sameAs:https://doi.org/10.1186/1471-2407-10-505
         keywords:
            Prostate Cancer
            Prostate Cancer Cell
            Luminal Cell
            Benign Tissue
            Prostate Cancer Tissue
            Cancer Research
            Oncology
            Surgical Oncology
            Health Promotion and Disease Prevention
            Biomedicine
            general
            Medicine/Public Health
         image:
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1186%2F1471-2407-10-505/MediaObjects/12885_2010_Article_2304_Fig1_HTML.jpg
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1186%2F1471-2407-10-505/MediaObjects/12885_2010_Article_2304_Fig2_HTML.jpg
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1186%2F1471-2407-10-505/MediaObjects/12885_2010_Article_2304_Fig3_HTML.jpg
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1186%2F1471-2407-10-505/MediaObjects/12885_2010_Article_2304_Fig4_HTML.jpg
         isPartOf:
            name:BMC Cancer
            issn:
               1471-2407
            volumeNumber:10
            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:Wolfgang A Schulz
               affiliation:
                     name:Heinrich Heine University
                     address:
                        name:Department of Urology, Heinrich Heine University, Düsseldorf, Germany
                        type:PostalAddress
                     type:Organization
               email:[email protected]
               type:Person
               name:Marc Ingenwerth
               affiliation:
                     name:Heinrich Heine University
                     address:
                        name:Department of Urology, Heinrich Heine University, Düsseldorf, Germany
                        type:PostalAddress
                     type:Organization
               type:Person
               name:Carolle E Djuidje
               affiliation:
                     name:Heinrich Heine University
                     address:
                        name:Department of Urology, Heinrich Heine University, Düsseldorf, Germany
                        type:PostalAddress
                     type:Organization
               type:Person
               name:Christiane Hader
               affiliation:
                     name:Heinrich Heine University
                     address:
                        name:Department of Urology, Heinrich Heine University, Düsseldorf, Germany
                        type:PostalAddress
                     type:Organization
               type:Person
               name:Jörg Rahnenführer
               affiliation:
                     name:University of Dortmund
                     address:
                        name:Department of Statistics, University of Dortmund, Dortmund, Germany
                        type:PostalAddress
                     type:Organization
               type:Person
               name:Rainer Engers
               affiliation:
                     name:Heinrich Heine University
                     address:
                        name:Department of Pathology, Heinrich Heine University, Düsseldorf, Germany
                        type:PostalAddress
                     type:Organization
               type:Person
         isAccessibleForFree:1
         type:ScholarlyArticle
      context:https://schema.org
ScholarlyArticle:
      headline:Changes in cortical cytoskeletal and extracellular matrix gene expression in prostate cancer are related to oncogenic ERG deregulation
      description:The cortical cytoskeleton network connects the actin cytoskeleton to various membrane proteins, influencing cell adhesion, polarity, migration and response to extracellular signals. Previous studies have suggested changes in the expression of specific components in prostate cancer, especially of 4.1 proteins (encoded by EPB41 genes) which form nodes in this network. Expression of EPB41L1, EPB41L2, EPB41L3 (protein: 4.1B), EPB41L4B (EHM2), EPB41L5, EPB49 (dematin), VIL2 (ezrin), and DLG1 (summarized as „cortical cytoskeleton" genes) as well as ERG was measured by quantitative RT-PCR in a well-characterized set of 45 M0 prostate adenocarcinoma and 13 benign tissues. Hypermethylation of EPB41L3 and GSTP1 was compared in 93 cancer tissues by methylation-specific PCR. Expression of 4.1B was further studied by immunohistochemistry. EPB41L1 and EPB41L3 were significantly downregulated and EPB41L4B was upregulated in cancer tissues. Low EPB41L1 or high EPB41L4B expression were associated with earlier biochemical recurrence. None of the other cortical cytoskeleton genes displayed expression changes, in particular EPB49 and VIL2, despite hints from previous studies. EPB41L3 downregulation was significantly associated with hypermethylation of its promoter and strongly correlated with GSTP1 hypermethylation. Protein 4.1B was detected most strongly in the basal cells of normal prostate epithelia. Its expression in carcinoma cells was similar to the weaker one in normal luminal cells. EPB41L3 downregulation and EPB41L4B upregulation were essentially restricted to the 22 cases with ERG overexpression. Expression changes in EPB41L3 and EPB41L4B closely paralleled those previously observed for the extracellular matrix genes FBLN1 and SPOCK1, respectively. Specific changes in the cortical cytoskeleton were observed during prostate cancer progression. They parallel changes in the expression of extracellular matrix components and all together appear to be associated with oncogenic ERG overexpression. We hypothesize that these alterations may contribute to the increased invasivity conferred to prostate cancer cells by ERG deregulation.
      datePublished:2010-09-22T00:00:00Z
      dateModified:2010-09-22T00:00:00Z
      pageStart:1
      pageEnd:9
      license:http://creativecommons.org/licenses/by/2.0
      sameAs:https://doi.org/10.1186/1471-2407-10-505
      keywords:
         Prostate Cancer
         Prostate Cancer Cell
         Luminal Cell
         Benign Tissue
         Prostate Cancer Tissue
         Cancer Research
         Oncology
         Surgical Oncology
         Health Promotion and Disease Prevention
         Biomedicine
         general
         Medicine/Public Health
      image:
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1186%2F1471-2407-10-505/MediaObjects/12885_2010_Article_2304_Fig1_HTML.jpg
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1186%2F1471-2407-10-505/MediaObjects/12885_2010_Article_2304_Fig2_HTML.jpg
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1186%2F1471-2407-10-505/MediaObjects/12885_2010_Article_2304_Fig3_HTML.jpg
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1186%2F1471-2407-10-505/MediaObjects/12885_2010_Article_2304_Fig4_HTML.jpg
      isPartOf:
         name:BMC Cancer
         issn:
            1471-2407
         volumeNumber:10
         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:Wolfgang A Schulz
            affiliation:
                  name:Heinrich Heine University
                  address:
                     name:Department of Urology, Heinrich Heine University, Düsseldorf, Germany
                     type:PostalAddress
                  type:Organization
            email:[email protected]
            type:Person
            name:Marc Ingenwerth
            affiliation:
                  name:Heinrich Heine University
                  address:
                     name:Department of Urology, Heinrich Heine University, Düsseldorf, Germany
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Carolle E Djuidje
            affiliation:
                  name:Heinrich Heine University
                  address:
                     name:Department of Urology, Heinrich Heine University, Düsseldorf, Germany
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Christiane Hader
            affiliation:
                  name:Heinrich Heine University
                  address:
                     name:Department of Urology, Heinrich Heine University, Düsseldorf, Germany
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Jörg Rahnenführer
            affiliation:
                  name:University of Dortmund
                  address:
                     name:Department of Statistics, University of Dortmund, Dortmund, Germany
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Rainer Engers
            affiliation:
                  name:Heinrich Heine University
                  address:
                     name:Department of Pathology, Heinrich Heine University, Düsseldorf, Germany
                     type:PostalAddress
                  type:Organization
            type:Person
      isAccessibleForFree:1
["Periodical","PublicationVolume"]:
      name:BMC Cancer
      issn:
         1471-2407
      volumeNumber:10
Organization:
      name:BioMed Central
      logo:
         url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
         type:ImageObject
      name:Heinrich Heine University
      address:
         name:Department of Urology, Heinrich Heine University, Düsseldorf, Germany
         type:PostalAddress
      name:Heinrich Heine University
      address:
         name:Department of Urology, Heinrich Heine University, Düsseldorf, Germany
         type:PostalAddress
      name:Heinrich Heine University
      address:
         name:Department of Urology, Heinrich Heine University, Düsseldorf, Germany
         type:PostalAddress
      name:Heinrich Heine University
      address:
         name:Department of Urology, Heinrich Heine University, Düsseldorf, Germany
         type:PostalAddress
      name:University of Dortmund
      address:
         name:Department of Statistics, University of Dortmund, Dortmund, Germany
         type:PostalAddress
      name:Heinrich Heine University
      address:
         name:Department of Pathology, Heinrich Heine University, Düsseldorf, Germany
         type:PostalAddress
ImageObject:
      url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
Person:
      name:Wolfgang A Schulz
      affiliation:
            name:Heinrich Heine University
            address:
               name:Department of Urology, Heinrich Heine University, Düsseldorf, Germany
               type:PostalAddress
            type:Organization
      email:[email protected]
      name:Marc Ingenwerth
      affiliation:
            name:Heinrich Heine University
            address:
               name:Department of Urology, Heinrich Heine University, Düsseldorf, Germany
               type:PostalAddress
            type:Organization
      name:Carolle E Djuidje
      affiliation:
            name:Heinrich Heine University
            address:
               name:Department of Urology, Heinrich Heine University, Düsseldorf, Germany
               type:PostalAddress
            type:Organization
      name:Christiane Hader
      affiliation:
            name:Heinrich Heine University
            address:
               name:Department of Urology, Heinrich Heine University, Düsseldorf, Germany
               type:PostalAddress
            type:Organization
      name:Jörg Rahnenführer
      affiliation:
            name:University of Dortmund
            address:
               name:Department of Statistics, University of Dortmund, Dortmund, Germany
               type:PostalAddress
            type:Organization
      name:Rainer Engers
      affiliation:
            name:Heinrich Heine University
            address:
               name:Department of Pathology, Heinrich Heine University, Düsseldorf, Germany
               type:PostalAddress
            type:Organization
PostalAddress:
      name:Department of Urology, Heinrich Heine University, Düsseldorf, Germany
      name:Department of Urology, Heinrich Heine University, Düsseldorf, Germany
      name:Department of Urology, Heinrich Heine University, Düsseldorf, Germany
      name:Department of Urology, Heinrich Heine University, Düsseldorf, Germany
      name:Department of Statistics, University of Dortmund, Dortmund, Germany
      name:Department of Pathology, Heinrich Heine University, Düsseldorf, Germany

External Links {🔗}(152)

Analytics and Tracking {📊}

Google Tag Manager

Libraries {📚}

Clipboard.js
Prism.js

CDN Services {📦}

Crossref

4.71s.

LINK . SPRINGER . COM {}