We are analyzing https://link.springer.com/article/10.1186/1471-2407-10-238.

Title:
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
Description:
Background 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
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Keywords {🔍}

resveratrol, cells, cancer, cell, igf, igfr, pubmed, colon, article, sirna, google, scholar, cas, proliferation, apoptosis, growth, levels, control, figure, treatment, results, suppression, signaling, protein, cycle, fkhrl, factor, suppresses, treated, activation, progression, pathway, human, suppressed, transcription, pathways, cyclin, similar, andor, insulinlike, colorectal, induced, effects, downstream, expression, central, authors, obesity, suppressing, effect,

Topics {✒️}

igf-1r/akt/wnt signaling pathways igf-1r/akt/gsk3β signaling pathway igf-i-induced tyrosine phosphorylation beta-catenin/tcf-4 complex imposes β-catenin/tcf-4 complex constitutes wnt/β-catenin signaling pathway wnt/β-catenin pathway plays igf-1r/akt/wnt pathways suppressing downstream igf-1r/akt dna damage-induced phosphorylation human igf-1r transcript wnt/beta-catenin signaling wnt/β-catenin signaling akt/gsk3β/wnt signaling wnt/β-catenin pathway [23] norad/igf2bp2/pdk1 pathway growth factor-1-induced phosphorylation igf-1r downstream signaling obesity-promoted colon cancer suppresses igf-1r levels blivet-van eggelpoel mj suppress igf-1r/akt anthracene-induced mammary carcinogenesis serine/threonine kinase akt phosphatidylinositol 3'-kinase/akt pathway nuclear β-catenin levels bcr-abl-expressing cells regulating igf-1r transcription growth factor-1-induced survival exhibited anti-proliferative properties activated igf-1r phosphorylates affecting igf-1r transcription obesity-enhanced colon cancer pre-publication history igf-1r sirna duplexes unlike igf-1r sirna tumor suppressor p53 goat anti-rabbit transcriptionally activates igf-1r induce anti-carcinogenic effects igf-1r promoter activity serum-free dmem/f-12 medium downregulating igf-1r levels related subjects phosphatidylinositol 3-kinase/akt kinase suppresses cell proliferation induced cell proliferation igf-1r sirna duplex igf-1r protein levels igf-1r constitutively active

Questions {❓}

How Many People Get Colorectal Cancer?

Schema {🗺️}

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 μM) 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
         pageEnd:14
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            Colon Cancer Cell
            Human Colon Cancer Cell
            Suppress Cell Proliferation
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            Oncology
            Surgical Oncology
            Health Promotion and Disease Prevention
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               affiliation:
                     name:Texas A&M University, College Station
                     address:
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ScholarlyArticle:
      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 μM) 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
      pageEnd:14
      license:http://creativecommons.org/licenses/by/2.0
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      keywords:
         Resveratrol
         Colon Cancer Cell
         Human Colon Cancer Cell
         Suppress Cell Proliferation
         Resveratrol Treatment
         Cancer Research
         Oncology
         Surgical Oncology
         Health Promotion and Disease Prevention
         Biomedicine
         general
         Medicine/Public Health
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         name:BioMed Central
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                     type:PostalAddress
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            affiliation:
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                  address:
                     name:Department of Food Science and Human Nutrition, 226 Gifford Building, Colorado State University, Fort Collins, USA
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Sridhar Radhakrishnan
            affiliation:
                  name:226 Gifford Building, Colorado State University
                  address:
                     name:Department of Food Science and Human Nutrition, 226 Gifford Building, Colorado State University, Fort Collins, USA
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Chris Tarver
            affiliation:
                  name:Texas A&M University, College Station
                  address:
                     name:Institute for Obesity Research and Program Evaluation, Texas A&M University, College Station, USA
                     type:PostalAddress
                  type:Organization
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      address:
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         type:PostalAddress
      name:226 Gifford Building, Colorado State University
      address:
         name:Department of Food Science and Human Nutrition, 226 Gifford Building, Colorado State University, Fort Collins, USA
         type:PostalAddress
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Person:
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      affiliation:
            name:226 Gifford Building, Colorado State University
            address:
               name:Department of Food Science and Human Nutrition, 226 Gifford Building, Colorado State University, Fort Collins, USA
               type:PostalAddress
            type:Organization
      email:[email protected]
      name:Lavanya Reddivari
      affiliation:
            name:226 Gifford Building, Colorado State University
            address:
               name:Department of Food Science and Human Nutrition, 226 Gifford Building, Colorado State University, Fort Collins, USA
               type:PostalAddress
            type:Organization
      name:Sridhar Radhakrishnan
      affiliation:
            name:226 Gifford Building, Colorado State University
            address:
               name:Department of Food Science and Human Nutrition, 226 Gifford Building, Colorado State University, Fort Collins, USA
               type:PostalAddress
            type:Organization
      name:Chris Tarver
      affiliation:
            name:Texas A&M University, College Station
            address:
               name:Institute for Obesity Research and Program Evaluation, Texas A&M University, College Station, USA
               type:PostalAddress
            type:Organization
PostalAddress:
      name:Department of Food Science and Human Nutrition, 226 Gifford Building, Colorado State University, Fort Collins, USA
      name:Department of Food Science and Human Nutrition, 226 Gifford Building, Colorado State University, Fort Collins, USA
      name:Department of Food Science and Human Nutrition, 226 Gifford Building, Colorado State University, Fort Collins, USA
      name:Institute for Obesity Research and Program Evaluation, Texas A&M University, College Station, USA

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