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  5. How Does Biomedcentral.com Make Money
  6. How Much Does Biomedcentral.com Make
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We began analyzing https://bmccancer.biomedcentral.com/articles/10.1186/1471-2407-11-49/peer-review, but it redirected us to https://bmccancer.biomedcentral.com/articles/10.1186/1471-2407-11-49/peer-review. The analysis below is for the second page.

Title[redir]:
Activation of β-catenin and Akt pathways by Twist are critical for the maintenance of EMT associated cancer stem cell-like characters | BMC Cancer | Peer Review
Description:
Epithelial-mesenchymal transition (EMT) not only confers tumor cells with a distinct advantage for metastatic dissemination, but also it provides those cells with cancer stem cell-like characters for proliferation and drug resistance. However, the molecular mechanism for maintenance of these stem cell-like traits remains unclear. In this study, we induced EMT in breast cancer MCF7 and cervical cancer Hela cells with expression of Twist, a key transcriptional factor of EMT. The morphological changes associated with EMT were analyzed by immunofluorescent staining and Western blotting. The stem cell-like traits associated with EMT were determined by tumorsphere-formation and expression of ALDH1 and CD44 in these cells. The activation of β-catenin and Akt pathways was examined by Western blotting and luciferase assays. We found that expression of Twist induced a morphological change associated with EMT. We also found that the cancer stem cell-like traits, such as tumorsphere formation, expression of ALDH1 and CD44, were significantly elevated in Twist-overexpressing cells. Interestingly, we showed that β-catenin and Akt pathways were activated in these Twist-overexpressing cells. Activation of β-catenin correlated with the expression of CD44. Knockdown of β-catenin expression and inhibition of the Akt pathway greatly suppressed the expression of CD44. Our results indicate that activation of β-catenin and Akt pathways are required for the sustention of EMT-associated stem cell-like traits.

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  • Education
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Content Management System {📝}

What CMS is biomedcentral.com built with?

Custom-built

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

Traffic Estimate {📈}

What is the average monthly size of biomedcentral.com audience?

🚀 Good Traffic: 50k - 100k visitors per month


Based on our best estimate, this website will receive around 50,019 visitors per month in the current month.
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How Does Biomedcentral.com Make Money? {💸}


Display Ads {🎯}


The website utilizes display ads within its content to generate revenue. Check the next section for further revenue estimates.

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How Much Does Biomedcentral.com Make? {💰}


Display Ads {🎯}

$690 per month
Our estimates place Biomedcentral.com's monthly online earnings from display ads at $462 to $1,271.

Keywords {🔍}

bmc, cookies, privacy, manuscript, reviewed, reviewer, report, author, version, jan, page, data, information, cancer, submission, submitted, dec, article, optional, content, personal, parties, policy, manage, published, peer, review, original, joana, paredes, hannah, harrison, responded, comments, binhua, zhou, resubmission, feb, contact, enquiries, editing, authors, choice, essential, make, site, function, advertising, personalisation, usage,

Topics {✒️}

authors scientific editing privacy choices/manage cookies cancer stem cell bmc european economic area state privacy rights accepting optional cookies peer review 1471-2407 contact manage preferences article published author responded personal data submission enquiries optional cookies data protection essential cookies cookies skip cookies policy privacy policy privacy statement usage analysis social media varying standards β-catenin akt pathways editorially accepted general enquiries preference centre springer nature content choices 1 feb 2011 privacy published choice make site function advertising personalisation consent processing parties information change accept activation twist critical

Schema {🗺️}

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         headline:Activation of β-catenin and Akt pathways by Twist are critical for the maintenance of EMT associated cancer stem cell-like characters
         description:Epithelial-mesenchymal transition (EMT) not only confers tumor cells with a distinct advantage for metastatic dissemination, but also it provides those cells with cancer stem cell-like characters for proliferation and drug resistance. However, the molecular mechanism for maintenance of these stem cell-like traits remains unclear. In this study, we induced EMT in breast cancer MCF7 and cervical cancer Hela cells with expression of Twist, a key transcriptional factor of EMT. The morphological changes associated with EMT were analyzed by immunofluorescent staining and Western blotting. The stem cell-like traits associated with EMT were determined by tumorsphere-formation and expression of ALDH1 and CD44 in these cells. The activation of β-catenin and Akt pathways was examined by Western blotting and luciferase assays. We found that expression of Twist induced a morphological change associated with EMT. We also found that the cancer stem cell-like traits, such as tumorsphere formation, expression of ALDH1 and CD44, were significantly elevated in Twist-overexpressing cells. Interestingly, we showed that β-catenin and Akt pathways were activated in these Twist-overexpressing cells. Activation of β-catenin correlated with the expression of CD44. Knockdown of β-catenin expression and inhibition of the Akt pathway greatly suppressed the expression of CD44. Our results indicate that activation of β-catenin and Akt pathways are required for the sustention of EMT-associated stem cell-like traits.
         datePublished:2011-02-01T00:00:00Z
         dateModified:2011-02-01T00:00:00Z
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            Wortmannin
            Salinomycin
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      headline:Activation of β-catenin and Akt pathways by Twist are critical for the maintenance of EMT associated cancer stem cell-like characters
      description:Epithelial-mesenchymal transition (EMT) not only confers tumor cells with a distinct advantage for metastatic dissemination, but also it provides those cells with cancer stem cell-like characters for proliferation and drug resistance. However, the molecular mechanism for maintenance of these stem cell-like traits remains unclear. In this study, we induced EMT in breast cancer MCF7 and cervical cancer Hela cells with expression of Twist, a key transcriptional factor of EMT. The morphological changes associated with EMT were analyzed by immunofluorescent staining and Western blotting. The stem cell-like traits associated with EMT were determined by tumorsphere-formation and expression of ALDH1 and CD44 in these cells. The activation of β-catenin and Akt pathways was examined by Western blotting and luciferase assays. We found that expression of Twist induced a morphological change associated with EMT. We also found that the cancer stem cell-like traits, such as tumorsphere formation, expression of ALDH1 and CD44, were significantly elevated in Twist-overexpressing cells. Interestingly, we showed that β-catenin and Akt pathways were activated in these Twist-overexpressing cells. Activation of β-catenin correlated with the expression of CD44. Knockdown of β-catenin expression and inhibition of the Akt pathway greatly suppressed the expression of CD44. Our results indicate that activation of β-catenin and Akt pathways are required for the sustention of EMT-associated stem cell-like traits.
      datePublished:2011-02-01T00:00:00Z
      dateModified:2011-02-01T00:00:00Z
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         MCF7 Cell
         Cancer Stem Cell
         Wortmannin
         Salinomycin
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         Surgical Oncology
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         general
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               type:PostalAddress
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      name:Departments of Molecular and Cellular Biochemistry, University of Kentucky School of Medicine, Lexington, USA
      name:Markey Cancer Center, University of Kentucky School of Medicine, Lexington, USA

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