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  4. Monthly Traffic Estimate
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  6. How Much Does Biomedcentral.com Make
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We began analyzing https://bmccancer.biomedcentral.com/articles/10.1186/1471-2407-10-238/peer-review, but it redirected us to https://bmccancer.biomedcentral.com/articles/10.1186/1471-2407-10-238/peer-review. The analysis below is for the second page.

Title[redir]:
Resveratrol suppresses IGF-1 induced human colon cancer cell proliferation and elevates apoptosis via suppression of IGF-1R/Wnt and activation of p53 signaling pathways | BMC Cancer | Peer Review
Description:
Obesity is a global phenomenon and is associated with various types of cancer, including colon cancer. There is a growing interest for safe and effective bioactive compounds that suppress the risk for obesity-promoted colon cancer. Resveratrol (trans-3, 4

Matching Content Categories {πŸ“š}

  • Social Networks
  • Technology & Computing
  • Non-Profit & Charity

Content Management System {πŸ“}

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 {πŸ“ˆ}

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

πŸš€ 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.
However, some sources were not loaded, we suggest to reload the page to get complete results.

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How Does Biomedcentral.com Make Money? {πŸ’Έ}


Display Ads {🎯}


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

Ads are managed by yourbow.com. Particular relationships are as follows:

Direct Advertisers (3)
yourbow.com, google.com, doceree.com

How Much Does Biomedcentral.com Make? {πŸ’°}


Display Ads {🎯}

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

Keywords {πŸ”}

bmc, cookies, version, privacy, manuscript, submitted, author, page, data, information, cancer, submission, resubmission, article, optional, content, personal, parties, policy, manage, published, peer, review, original, reviewed, reviewer, report, randall, holcombe, mar, responded, comments, jairam, vanamala, contact, enquiries, editing, authors, choice, essential, make, site, function, advertising, personalisation, usage, analysis, social, media, accepting,

Topics {βœ’οΈ}

authors scientific editing privacy choices/manage cookies igf-1r/wnt bmc european economic area state privacy rights accepting optional cookies peer review 1471-2407 contact manage preferences article published submission enquiries author responded personal data optional cookies data protection essential cookies cookies skip cookies policy privacy policy privacy statement usage analysis social media varying standards elevates apoptosis editorially accepted general enquiries preference centre springer nature content choices privacy published choice make site function advertising personalisation consent processing parties information change accept suppression activation submitted reviewed find

Schema {πŸ—ΊοΈ}

WebPage:
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         headline:Resveratrol suppresses IGF-1 induced human colon cancer cell proliferation and elevates apoptosis via suppression of IGF-1R/Wnt and activation of p53 signaling pathways
         description:Obesity is a global phenomenon and is associated with various types of cancer, including colon cancer. There is a growing interest for safe and effective bioactive compounds that suppress the risk for obesity-promoted colon cancer. Resveratrol (trans-3, 4', 5,-trihydroxystilbene), a stilbenoid found in the skin of red grapes and peanuts suppresses many types of cancers by regulating cell proliferation and apoptosis through a variety of mechanisms, however, resveratrol effects on obesity-promoted colon cancer are not clearly established. We investigated the anti-proliferative effects of resveratrol on HT-29 and SW480 human colon cancer cells in the presence and absence of insulin like growth factor-1 (IGF-1; elevated during obesity) and elucidated the mechanisms of action using IGF-1R siRNA in HT-29 cells which represents advanced colon carcinogenesis. Resveratrol (100-150 ΞΌM) exhibited anti-proliferative properties in HT-29 cells even after IGF-1 exposure by arresting G0/G1-S phase cell cycle progression through p27 stimulation and cyclin D1 suppression. Treatment with resveratrol suppressed IGF-1R protein levels and concurrently attenuated the downstream Akt/Wnt signaling pathways that play a critical role in cell proliferation. Targeted suppression of IGF-1R using IGF-1R siRNA also affected these signaling pathways in a similar manner. Resveratrol treatment induced apoptosis by activating tumor suppressor p53 protein, whereas IGF-1R siRNA treatment did not affect apoptosis. Our data suggests that resveratrol not only suppresses cell proliferation by inhibiting IGF-1R and its downstream signaling pathways similar to that of IGF-1R siRNA but also enhances apoptosis via activation of the p53 pathway. For the first time, we report that resveratrol suppresses colon cancer cell proliferation and elevates apoptosis even in the presence of IGF-1 via suppression of IGF-1R/Akt/Wnt signaling pathways and activation of p53, suggesting its potential role as a chemotherapeutic agent.
         datePublished:2010-05-26T00:00:00Z
         dateModified:2010-05-26T00:00:00Z
         pageStart:1
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         license:http://creativecommons.org/licenses/by/2.0
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      headline:Resveratrol suppresses IGF-1 induced human colon cancer cell proliferation and elevates apoptosis via suppression of IGF-1R/Wnt and activation of p53 signaling pathways
      description:Obesity is a global phenomenon and is associated with various types of cancer, including colon cancer. There is a growing interest for safe and effective bioactive compounds that suppress the risk for obesity-promoted colon cancer. Resveratrol (trans-3, 4', 5,-trihydroxystilbene), a stilbenoid found in the skin of red grapes and peanuts suppresses many types of cancers by regulating cell proliferation and apoptosis through a variety of mechanisms, however, resveratrol effects on obesity-promoted colon cancer are not clearly established. We investigated the anti-proliferative effects of resveratrol on HT-29 and SW480 human colon cancer cells in the presence and absence of insulin like growth factor-1 (IGF-1; elevated during obesity) and elucidated the mechanisms of action using IGF-1R siRNA in HT-29 cells which represents advanced colon carcinogenesis. Resveratrol (100-150 ΞΌM) exhibited anti-proliferative properties in HT-29 cells even after IGF-1 exposure by arresting G0/G1-S phase cell cycle progression through p27 stimulation and cyclin D1 suppression. Treatment with resveratrol suppressed IGF-1R protein levels and concurrently attenuated the downstream Akt/Wnt signaling pathways that play a critical role in cell proliferation. Targeted suppression of IGF-1R using IGF-1R siRNA also affected these signaling pathways in a similar manner. Resveratrol treatment induced apoptosis by activating tumor suppressor p53 protein, whereas IGF-1R siRNA treatment did not affect apoptosis. Our data suggests that resveratrol not only suppresses cell proliferation by inhibiting IGF-1R and its downstream signaling pathways similar to that of IGF-1R siRNA but also enhances apoptosis via activation of the p53 pathway. For the first time, we report that resveratrol suppresses colon cancer cell proliferation and elevates apoptosis even in the presence of IGF-1 via suppression of IGF-1R/Akt/Wnt signaling pathways and activation of p53, suggesting its potential role as a chemotherapeutic agent.
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         Human Colon Cancer Cell
         Suppress Cell Proliferation
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         Health Promotion and Disease Prevention
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      name:Department of Food Science and Human Nutrition, 226 Gifford Building, Colorado State University, Fort Collins, USA
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