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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. Questions
  9. Schema
  10. Social Networks
  11. External Links
  12. Analytics And Tracking
  13. Libraries
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We began analyzing https://www.tandfonline.com/doi/full/10.1080/19336918.2016.1221567, but it redirected us to https://www.tandfonline.com/doi/full/10.1080/19336918.2016.1221567. The analysis below is for the second page.

Title[redir]:
Full article: Estrogen-related receptor α participates transforming growth factor-β (TGF-β) induced epithelial-mesenchymal transition of osteosarcoma cells
Description:
Osteosarcoma, which develops from primitive transformed cells of mesenchymal origin, is the most common histological form of primary bone cancer.21 Half of the osteosarcoma patients often exhibit p...

Matching Content Categories {📚}

  • Science
  • Education
  • Dating & Relationships

Content Management System {📝}

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 {📈}

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 9,135,289 visitors per month in the current month.

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How Does Doi.org Make Money? {💸}

We find it hard to spot revenue streams.

While profit motivates many websites, others exist to inspire, entertain, or provide valuable resources. Websites have a variety of goals. And this might be one of them. Doi.org might be cashing in, but we can't detect the method they're using.

Keywords {🔍}

cells, open, tgfβ, osteosarcoma, snail, errα, emt, expression, science, windowgoogle, scholar, windowweb, cell, induced, windowpubmed, hos, cancer, treatment, pmid, tfgβ, results, studies, ecad, regulation, fig, qrtpcr, significantly, vim, treated, ngml, data, metastasis, transcription, mrna, journals, vitro, nuclear, sciences, permissions, suggested, sierrα, receptor, invasion, epithelial, trigger, analyzed, reverse, access, search, growth,

Topics {✒️}

social care medicine transforming growth factor-β estrogen-related receptors α sun yat-sen unviersity sun yat-sen university google scholar reprints attenuate tfg-β induced tfg-β induced emt attenuate tgf-β induced tfg-β induced transcription hrp-conjugated secondary antibodies induced epithelial-mesenchymal transition tgf-β-induced epithelial orphan nuclear receptor estrogen receptor signaling methods cell culture tgf-β induced emt emt-related transcription factors uncovered wound area google scholar kudo-saito pi3k/akt signaling pathway tgf-β significantly decreased estrogen-related receptors chamber-based invasion assay display full size tgf-β-induced expression quantitative real-time pcr results tgf-β triggers tfg-β induced confer methotrexate resistance receive personalised research epithelial characteristics e-cadherin request academic permissions de herreros ag estrogen receptor emt related markers tgf-β induced references ao twitter page taylor estrogen promotes apoptosis francis group e-cadherin gene expression tgf-β increases date register e-cad gene promoter journal search calls transcription factor snail comparative ct method negative control si-rna estrogen response elements

Questions {❓}

  • Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?
  • Snail, ZEB and bHLH factors in tumour progression: an alliance against the epithelial phenotype?
  • Why publish with us?

Schema {🗺️}

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            name:Estrogen-related receptor α participates ....
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      position:1
      name:Home
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      position:2
      name:All Journals
      item:https://www.tandfonline.com/action/showPublications?pubType=journal
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      name:Volume 11, Issue 4
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      name:Estrogen-related receptor α participates ....
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      url:https://www.tandfonline.com/doi/full/10.1080/19336918.2016.1221567
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      articleSection:Research Paper
      name:Estrogen-related receptor α participates transforming growth factor-β (TGF-β) induced epithelial-mesenchymal transition of osteosarcoma cells
      headline:Estrogen-related receptor α participates transforming growth factor-β (TGF-β) induced epithelial-mesenchymal transition of osteosarcoma cells
      abstract:Osteosarcoma patients often exhibit pulmonary metastasis, which results in high patient mortality. Understanding the mechanisms of advanced metastasis in osteosarcoma cell is important for the targeted treatment and drug development. Our present study revealed that transforming growth factor-β (TGF-β) treatment can significantly promote the in vitro migration and invasion of human osteosarcoma MG-63 and HOS cells. The loss of epithelial characteristics E-cadherin (E-Cad) and up regulation of mesenchymal markers Vimentin (Vim) suggested TGF-β induced epithelial-mesenchymal transition (EMT) of osteosarcoma cells. TGF-β treatment obviously increased the expression of Snail, a key EMT-related transcription factor, in both MG-63 and HOS cells. Silencing of Snail markedly attenuated TGF-β induced down regulation of E-cad and up regulation of Vim. TGF-β treatment also significantly increased the expression and nuclear translocation of estrogen-related receptors α (ERRα), while had no obvious effect on the expression of ERα, ERβ, or ERRγ. Knock down of ERRα or its inhibitor XCT-790 significantly attenuated TFG-β induced EMT and transcription of Snail in osteosarcoma cells. Collectively, our present study revealed that TGF-β treatment can trigger the EMT of osteosarcoma cells via ERRα/Snail pathways. Our data suggested that ERRα/Snail pathways might be potential therapeutic targets of metastasis of osteosarcoma cells.
      description:Osteosarcoma patients often exhibit pulmonary metastasis, which results in high patient mortality. Understanding the mechanisms of advanced metastasis in osteosarcoma cell is important for the targeted treatment and drug development. Our present study revealed that transforming growth factor-β (TGF-β) treatment can significantly promote the in vitro migration and invasion of human osteosarcoma MG-63 and HOS cells. The loss of epithelial characteristics E-cadherin (E-Cad) and up regulation of mesenchymal markers Vimentin (Vim) suggested TGF-β induced epithelial-mesenchymal transition (EMT) of osteosarcoma cells. TGF-β treatment obviously increased the expression of Snail, a key EMT-related transcription factor, in both MG-63 and HOS cells. Silencing of Snail markedly attenuated TGF-β induced down regulation of E-cad and up regulation of Vim. TGF-β treatment also significantly increased the expression and nuclear translocation of estrogen-related receptors α (ERRα), while had no obvious effect on the expression of ERα, ERβ, or ERRγ. Knock down of ERRα or its inhibitor XCT-790 significantly attenuated TFG-β induced EMT and transcription of Snail in osteosarcoma cells. Collectively, our present study revealed that TGF-β treatment can trigger the EMT of osteosarcoma cells via ERRα/Snail pathways. Our data suggested that ERRα/Snail pathways might be potential therapeutic targets of metastasis of osteosarcoma cells.
      author:
            type:Person
            name:Yantao Chen
            type:Person
            name:Kunshui Zhang
            type:Person
            name:Yang Li
            type:Person
            name:Qing He
      keywords:EMT, ERRα, osteosarcoma, Snail, TGF-β
      pageStart:338
      pageEnd:346
      datePublished:2016-08-30
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      name:Yang Li
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External Links {🔗}(205)

Analytics and Tracking {📊}

  • Google Analytics
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Libraries {📚}

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Emails and Hosting {✉️}

Mail Servers:

  • mx.zoho.eu
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Name Servers:

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CDN Services {📦}

  • Cookielaw
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