Here's how DOI.ORG makes money* and how much!

*Please read our disclaimer before using our estimates.
Loading...

DOI . ORG {}

  1. Analyzed Page
  2. Matching Content Categories
  3. CMS
  4. Monthly Traffic Estimate
  5. How Does Doi.org Make Money
  6. Keywords
  7. Topics
  8. Schema
  9. Social Networks
  10. External Links
  11. Analytics And Tracking
  12. Libraries
  13. Hosting Providers
  14. CDN Services

We began analyzing https://www.nature.com/articles/1204920, but it redirected us to https://www.nature.com/articles/1204920. The analysis below is for the second page.

Title[redir]:
Regulation of breast cancer cell motility by insulin receptor substrate-2 (IRS-2) in metastatic variants of human breast cancer cell lines | Oncogene
Description:
Insulin-like growth factors (IGFs) regulate breast cancer cell proliferation, protect cells from apoptosis, and enhance metastasis. In this study, we examined the IGF signaling pathway in two breast cancer cell lines selected for metastatic behavior. LCC6 was selected for growth as an ascites tumor in athymic mice from parental MDA-MB-435 cells (435P). The MDA-231BO cell line was derived from osseous metastases that formed after intracardiac injection of the MDA-MB-231 cell line in athymic mice. Compared to the parental cell lines, IGF-I treatment enhanced IRS-2 phosphorylation over IRS-1 in the metastatic variants. IGF-I stimulated cell migration in the variant cells, but not in the parental cells. To determine the role for IRS-2 in IGF-mediated motility, we transfected MDA-231BO cells with an anti-sense IRS-2 construct. Transfected cells had decreased levels of IRS-2 with diminished IGF-mediated motility and anchorage independent growth when compared to control cells. However, adherence to fibronectin was enhanced in the transfected cells compared to MDA-231BO cells. Our data show that breast cancer cells selected for metastatic behavior in vivo have increased IRS-2 activation and signaling. In these cells, IGF-I enhances cell adhesion and motility suggesting that IRS-2 may mediate these aspects of the malignant phenotype.

Matching Content Categories {πŸ“š}

  • Telecommunications
  • Science
  • Education

Content Management System {πŸ“}

What CMS is doi.org built with?

Custom-built

No common CMS systems were detected on Doi.org, and no known web development framework was identified.

Traffic Estimate {πŸ“ˆ}

What is the average monthly size of doi.org 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 Doi.org Make Money? {πŸ’Έ}

We don’t know how the website earns money.

While many websites aim to make money, others are created to share knowledge or showcase creativity. People build websites for various reasons. This could be one of them. Doi.org could be getting rich in stealth mode, or the way it's monetizing isn't detectable.

Keywords {πŸ”}

cancer, cell, article, breast, nature, cells, biol, irs, yee, access, res, receptor, insulin, google, scholar, content, substrate, jackson, growth, chem, cas, cookies, oncogene, privacy, data, motility, metastatic, yoneda, open, journal, november, lines, insulinlike, parental, igfi, lee, texas, san, antonio, advertising, information, subscribe, variants, james, zhang, douglas, signaling, selected, mdamb, mdabo,

Topics {βœ’οΈ}

nature portfolio permissions reprints privacy policy nature public health service immune prognostic index advertising social media author information authors glycolysis-related gene signature author correspondence mda-231bo cell line mda-mb-231 cell line diminished igf-mediated motility anti-sense irs-2 construct parental mda-mb-435 cells transfected mda-231bo cells springerlink instant access permissions insulin receptor substrate-2 insulin receptor substrate-1 insulin receptor substrate-4 personal data stimulated cell migration enhances cell adhesion data protection data show parental cell lines high-risk patients mda-231bo cells privacy mda-mb-435 parental issue learn igf-mediated motility breast cancer explore content subscription content drs robert clark anchorage independent growth european economic area institutional subscriptions read le marchand-brustel val toledo-loboluis accepting optional cookies journals search log de frias dv igf signaling pathway converting signaling dynamics growth factors manage preferences

Schema {πŸ—ΊοΈ}

WebPage:
      mainEntity:
         headline:Regulation of breast cancer cell motility by insulin receptor substrate-2 (IRS-2) in metastatic variants of human breast cancer cell lines
         description:Insulin-like growth factors (IGFs) regulate breast cancer cell proliferation, protect cells from apoptosis, and enhance metastasis. In this study, we examined the IGF signaling pathway in two breast cancer cell lines selected for metastatic behavior. LCC6 was selected for growth as an ascites tumor in athymic mice from parental MDA-MB-435 cells (435P). The MDA-231BO cell line was derived from osseous metastases that formed after intracardiac injection of the MDA-MB-231 cell line in athymic mice. Compared to the parental cell lines, IGF-I treatment enhanced IRS-2 phosphorylation over IRS-1 in the metastatic variants. IGF-I stimulated cell migration in the variant cells, but not in the parental cells. To determine the role for IRS-2 in IGF-mediated motility, we transfected MDA-231BO cells with an anti-sense IRS-2 construct. Transfected cells had decreased levels of IRS-2 with diminished IGF-mediated motility and anchorage independent growth when compared to control cells. However, adherence to fibronectin was enhanced in the transfected cells compared to MDA-231BO cells. Our data show that breast cancer cells selected for metastatic behavior in vivo have increased IRS-2 activation and signaling. In these cells, IGF-I enhances cell adhesion and motility suggesting that IRS-2 may mediate these aspects of the malignant phenotype.
         datePublished:2001-11-16T00:00:00Z
         dateModified:2001-11-16T00:00:00Z
         pageStart:7318
         pageEnd:7325
         sameAs:https://doi.org/10.1038/sj.onc.1204920
         keywords:
            breast neoplasms
            insulin-like growth factors
            cell migration
            insulin receptor substrate
            adhesion
            Medicine/Public Health
            general
            Internal Medicine
            Cell Biology
            Human Genetics
            Oncology
            Apoptosis
         image:
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1038%2Fsj.onc.1204920/MediaObjects/41388_2001_Article_BF1204920_Fig1_HTML.jpg
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1038%2Fsj.onc.1204920/MediaObjects/41388_2001_Article_BF1204920_Fig2_HTML.jpg
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1038%2Fsj.onc.1204920/MediaObjects/41388_2001_Article_BF1204920_Fig3_HTML.jpg
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1038%2Fsj.onc.1204920/MediaObjects/41388_2001_Article_BF1204920_Fig4_HTML.jpg
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1038%2Fsj.onc.1204920/MediaObjects/41388_2001_Article_BF1204920_Fig5_HTML.jpg
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1038%2Fsj.onc.1204920/MediaObjects/41388_2001_Article_BF1204920_Fig6_HTML.jpg
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1038%2Fsj.onc.1204920/MediaObjects/41388_2001_Article_BF1204920_Fig7_HTML.jpg
         isPartOf:
            name:Oncogene
            issn:
               1476-5594
               0950-9232
            volumeNumber:20
            type:
               Periodical
               PublicationVolume
         publisher:
            name:Nature Publishing Group UK
            logo:
               url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
               type:ImageObject
            type:Organization
         author:
               name:James G Jackson
               affiliation:
                     name:University of Texas Health Science Center at San Antonio
                     address:
                        name:Department of Medicine, Division of Medical Oncology, University of Texas Health Science Center at San Antonio, San Antonio, USA
                        type:PostalAddress
                     type:Organization
               type:Person
               name:Xihong Zhang
               affiliation:
                     name:Oncology, and Transplantation, University of Minnesota
                     address:
                        name:Department of Medicine, Division of Hematology, Oncology, and Transplantation, University of Minnesota, Minneapolis, USA
                        type:PostalAddress
                     type:Organization
               type:Person
               name:Toshiyuki Yoneda
               affiliation:
                     name:University of Texas Health Science Center at San Antonio
                     address:
                        name:Department of Medicine, Division of Endocrinology, University of Texas Health Science Center at San Antonio, San Antonio, USA
                        type:PostalAddress
                     type:Organization
               type:Person
               name:Douglas Yee
               affiliation:
                     name:Oncology, and Transplantation, University of Minnesota
                     address:
                        name:Department of Medicine, Division of Hematology, Oncology, and Transplantation, University of Minnesota, Minneapolis, USA
                        type:PostalAddress
                     type:Organization
               email:[email protected]
               type:Person
         isAccessibleForFree:
         hasPart:
            isAccessibleForFree:
            cssSelector:.main-content
            type:WebPageElement
         type:ScholarlyArticle
      context:https://schema.org
ScholarlyArticle:
      headline:Regulation of breast cancer cell motility by insulin receptor substrate-2 (IRS-2) in metastatic variants of human breast cancer cell lines
      description:Insulin-like growth factors (IGFs) regulate breast cancer cell proliferation, protect cells from apoptosis, and enhance metastasis. In this study, we examined the IGF signaling pathway in two breast cancer cell lines selected for metastatic behavior. LCC6 was selected for growth as an ascites tumor in athymic mice from parental MDA-MB-435 cells (435P). The MDA-231BO cell line was derived from osseous metastases that formed after intracardiac injection of the MDA-MB-231 cell line in athymic mice. Compared to the parental cell lines, IGF-I treatment enhanced IRS-2 phosphorylation over IRS-1 in the metastatic variants. IGF-I stimulated cell migration in the variant cells, but not in the parental cells. To determine the role for IRS-2 in IGF-mediated motility, we transfected MDA-231BO cells with an anti-sense IRS-2 construct. Transfected cells had decreased levels of IRS-2 with diminished IGF-mediated motility and anchorage independent growth when compared to control cells. However, adherence to fibronectin was enhanced in the transfected cells compared to MDA-231BO cells. Our data show that breast cancer cells selected for metastatic behavior in vivo have increased IRS-2 activation and signaling. In these cells, IGF-I enhances cell adhesion and motility suggesting that IRS-2 may mediate these aspects of the malignant phenotype.
      datePublished:2001-11-16T00:00:00Z
      dateModified:2001-11-16T00:00:00Z
      pageStart:7318
      pageEnd:7325
      sameAs:https://doi.org/10.1038/sj.onc.1204920
      keywords:
         breast neoplasms
         insulin-like growth factors
         cell migration
         insulin receptor substrate
         adhesion
         Medicine/Public Health
         general
         Internal Medicine
         Cell Biology
         Human Genetics
         Oncology
         Apoptosis
      image:
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1038%2Fsj.onc.1204920/MediaObjects/41388_2001_Article_BF1204920_Fig1_HTML.jpg
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1038%2Fsj.onc.1204920/MediaObjects/41388_2001_Article_BF1204920_Fig2_HTML.jpg
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1038%2Fsj.onc.1204920/MediaObjects/41388_2001_Article_BF1204920_Fig3_HTML.jpg
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1038%2Fsj.onc.1204920/MediaObjects/41388_2001_Article_BF1204920_Fig4_HTML.jpg
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1038%2Fsj.onc.1204920/MediaObjects/41388_2001_Article_BF1204920_Fig5_HTML.jpg
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1038%2Fsj.onc.1204920/MediaObjects/41388_2001_Article_BF1204920_Fig6_HTML.jpg
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1038%2Fsj.onc.1204920/MediaObjects/41388_2001_Article_BF1204920_Fig7_HTML.jpg
      isPartOf:
         name:Oncogene
         issn:
            1476-5594
            0950-9232
         volumeNumber:20
         type:
            Periodical
            PublicationVolume
      publisher:
         name:Nature Publishing Group UK
         logo:
            url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
            type:ImageObject
         type:Organization
      author:
            name:James G Jackson
            affiliation:
                  name:University of Texas Health Science Center at San Antonio
                  address:
                     name:Department of Medicine, Division of Medical Oncology, University of Texas Health Science Center at San Antonio, San Antonio, USA
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Xihong Zhang
            affiliation:
                  name:Oncology, and Transplantation, University of Minnesota
                  address:
                     name:Department of Medicine, Division of Hematology, Oncology, and Transplantation, University of Minnesota, Minneapolis, USA
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Toshiyuki Yoneda
            affiliation:
                  name:University of Texas Health Science Center at San Antonio
                  address:
                     name:Department of Medicine, Division of Endocrinology, University of Texas Health Science Center at San Antonio, San Antonio, USA
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Douglas Yee
            affiliation:
                  name:Oncology, and Transplantation, University of Minnesota
                  address:
                     name:Department of Medicine, Division of Hematology, Oncology, and Transplantation, University of Minnesota, Minneapolis, USA
                     type:PostalAddress
                  type:Organization
            email:[email protected]
            type:Person
      isAccessibleForFree:
      hasPart:
         isAccessibleForFree:
         cssSelector:.main-content
         type:WebPageElement
["Periodical","PublicationVolume"]:
      name:Oncogene
      issn:
         1476-5594
         0950-9232
      volumeNumber:20
Organization:
      name:Nature Publishing Group UK
      logo:
         url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
         type:ImageObject
      name:University of Texas Health Science Center at San Antonio
      address:
         name:Department of Medicine, Division of Medical Oncology, University of Texas Health Science Center at San Antonio, San Antonio, USA
         type:PostalAddress
      name:Oncology, and Transplantation, University of Minnesota
      address:
         name:Department of Medicine, Division of Hematology, Oncology, and Transplantation, University of Minnesota, Minneapolis, USA
         type:PostalAddress
      name:University of Texas Health Science Center at San Antonio
      address:
         name:Department of Medicine, Division of Endocrinology, University of Texas Health Science Center at San Antonio, San Antonio, USA
         type:PostalAddress
      name:Oncology, and Transplantation, University of Minnesota
      address:
         name:Department of Medicine, Division of Hematology, Oncology, and Transplantation, University of Minnesota, Minneapolis, USA
         type:PostalAddress
ImageObject:
      url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
Person:
      name:James G Jackson
      affiliation:
            name:University of Texas Health Science Center at San Antonio
            address:
               name:Department of Medicine, Division of Medical Oncology, University of Texas Health Science Center at San Antonio, San Antonio, USA
               type:PostalAddress
            type:Organization
      name:Xihong Zhang
      affiliation:
            name:Oncology, and Transplantation, University of Minnesota
            address:
               name:Department of Medicine, Division of Hematology, Oncology, and Transplantation, University of Minnesota, Minneapolis, USA
               type:PostalAddress
            type:Organization
      name:Toshiyuki Yoneda
      affiliation:
            name:University of Texas Health Science Center at San Antonio
            address:
               name:Department of Medicine, Division of Endocrinology, University of Texas Health Science Center at San Antonio, San Antonio, USA
               type:PostalAddress
            type:Organization
      name:Douglas Yee
      affiliation:
            name:Oncology, and Transplantation, University of Minnesota
            address:
               name:Department of Medicine, Division of Hematology, Oncology, and Transplantation, University of Minnesota, Minneapolis, USA
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Department of Medicine, Division of Medical Oncology, University of Texas Health Science Center at San Antonio, San Antonio, USA
      name:Department of Medicine, Division of Hematology, Oncology, and Transplantation, University of Minnesota, Minneapolis, USA
      name:Department of Medicine, Division of Endocrinology, University of Texas Health Science Center at San Antonio, San Antonio, USA
      name:Department of Medicine, Division of Hematology, Oncology, and Transplantation, University of Minnesota, Minneapolis, USA
WebPageElement:
      isAccessibleForFree:
      cssSelector:.main-content

Social Networks {πŸ‘}(1)

External Links {πŸ”—}(124)

Analytics and Tracking {πŸ“Š}

  • Google Tag Manager

Libraries {πŸ“š}

  • Prism.js
  • Zoom.js

Emails and Hosting {βœ‰οΈ}

Mail Servers:

  • mx.zoho.eu
  • mx2.zoho.eu
  • mx3.zoho.eu

Name Servers:

  • josh.ns.cloudflare.com
  • zita.ns.cloudflare.com

CDN Services {πŸ“¦}

  • Crossref

3.96s.