We are analyzing https://link.springer.com/article/10.1007/s12307-011-0087-2.

Title:
Adipocytes Promote B16BL6 Melanoma Cell Invasion and the Epithelial-to-Mesenchymal Transition | Cancer Microenvironment
Description:
Metastatic melanoma is one of the most deadly and evasive types of cancer. On average, cancer patients with metastatic melanoma survive only 6–9 months after diagnosis. Epidemiological and animal studies suggest that obesity increases the metastatic ability of malignant melanoma, though the mechanism is not known. In the present studies, we assessed the ability of 3T3L1 adipocytes to modulate B16BL6 melanoma cell invasion and the Epithelial-to-Mesenchymal Transition (EMT). For this purpose, we induced the differentiation of 3T3L1 fibroblasts to adipocytes. Then, we collected the cell culture media from both fibroblasts and adipocytes and determined their effect on the invasive ability and EMT gene expression of B16BL6 melanoma cells. Results show that adipocyte media increased that ability of B16BL6 cells to invade. The higher invasive ability of B16BL6 melanoma cells was associated with increased expression of EMT genes such as Snai1, MMP9, Twist, and Vimentin. Additionally, the expression of the cell-to-cell adhesion protein E-cadherin and the metastasis suppressor gene Kiss1 were down-regulated in these B16BL6 cells. Also, adipocytes had high levels of the pro-inflammatory cytokine Interleukin 6 (IL-6). Treatment of B16BL6 cells with IL-6 elicited similar effects as the adipocyte media; IL-6 promoted the invasive ability of B16BL6 melanoma cells, increased the expression of Snai1, and decreased Kiss1 expression. IL-6 neutralization, however, did not have a visible effect on adipocyte media-induced invasion and snai1 staining. In summary, adipocytes may increase the invasive ability of B16BL6 melanoma cells by promoting EMT and decreasing the expression of genes such as E-cadherin and Kiss1.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {📚}

Education
Science
Telecommunications

Content Management System {📝}

What CMS is link.springer.com built with?

Custom-built

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

Traffic Estimate {📈}

What is the average monthly size of link.springer.com audience?

🌠 Phenomenal Traffic: 5M - 10M visitors per month

Based on our best estimate, this website will receive around 7,626,182 visitors per month in the current month.

check SE Ranking
check Ahrefs
check Similarweb
check Ubersuggest
check Semrush

How Does Link.springer.com Make Money? {💸}

We find it hard to spot revenue streams.

Not all websites are made for profit; some exist to inform or educate users. Or any other reason why people make websites. And this might be the case. Link.springer.com might be plotting its profit, but the way they're doing it isn't detectable yet.

Keywords {🔍}

article, google, scholar, cas, pubmed, cancer, cell, melanoma, cells, expression, transition, metastasis, adipocytes, bbl, epithelialmesenchymal, tumor, biol, microenvironment, invasion, ability, gene, canc, kiss, access, progression, usa, austin, privacy, cookies, content, epithelialtomesenchymal, malignant, emt, adipocyte, role, epithelial, biochem, media, publish, search, nomelí, núñez, metastatic, obesity, induced, differentiation, fibroblasts, invasive, genes, snai,

Topics {✒️}

inflammation-induced cell migration 3t3-l1 pre-adipocyte differentiation adipocyte media-induced invasion tgf-beta promotes invasion epithelial-mesenchymal transition induced month download article/chapter tgf-beta-induced epithelial epithelial-mesenchymal transition phenotype transforming growth factor-beta p65/p50 nuclear translocation 3t3-l1 adipocyte differentiation induce pd-l1 expression e-cadherin gene expression epithelial-mesenchymal transition obesity-related inflammatory diseases full article pdf b16bl6 melanoma cells epithelial-mesenchymal transitions melanoma cancer microenvironment cancer cell metastasis privacy choices/manage cookies pathway mediates motility gastric cancer cells emt gene expression mesenchymal transition mesenchymal transition cell culture media wnt5a/protein kinase decreased kiss1 expression 3t3l1 adipocytes embryonic transcription factor adipocyte media increased metastatic melanoma survive circulating tumor cells breast cancer article kushiro severe pulmonary metastasis agricultural health study metastasis suppressors alter european economic area body mass index jnk signal pathways molecular targeted therapy increasing fascin1 expression conditions privacy policy snail transcription factor animal studies suggest high-throughput study regulating nf-kappa tumor progression

Questions {❓}

Peinado H, Olmeda D, Cano A (2007) Snail, Zeb and bHLH factors in tumour progression: an alliance against the epithelial phenotype?

Schema {🗺️}

WebPage:
      mainEntity:
         headline:Adipocytes Promote B16BL6 Melanoma Cell Invasion and the Epithelial-to-Mesenchymal Transition
         description:Metastatic melanoma is one of the most deadly and evasive types of cancer. On average, cancer patients with metastatic melanoma survive only 6–9 months after diagnosis. Epidemiological and animal studies suggest that obesity increases the metastatic ability of malignant melanoma, though the mechanism is not known. In the present studies, we assessed the ability of 3T3L1 adipocytes to modulate B16BL6 melanoma cell invasion and the Epithelial-to-Mesenchymal Transition (EMT). For this purpose, we induced the differentiation of 3T3L1 fibroblasts to adipocytes. Then, we collected the cell culture media from both fibroblasts and adipocytes and determined their effect on the invasive ability and EMT gene expression of B16BL6 melanoma cells. Results show that adipocyte media increased that ability of B16BL6 cells to invade. The higher invasive ability of B16BL6 melanoma cells was associated with increased expression of EMT genes such as Snai1, MMP9, Twist, and Vimentin. Additionally, the expression of the cell-to-cell adhesion protein E-cadherin and the metastasis suppressor gene Kiss1 were down-regulated in these B16BL6 cells. Also, adipocytes had high levels of the pro-inflammatory cytokine Interleukin 6 (IL-6). Treatment of B16BL6 cells with IL-6 elicited similar effects as the adipocyte media; IL-6 promoted the invasive ability of B16BL6 melanoma cells, increased the expression of Snai1, and decreased Kiss1 expression. IL-6 neutralization, however, did not have a visible effect on adipocyte media-induced invasion and snai1 staining. In summary, adipocytes may increase the invasive ability of B16BL6 melanoma cells by promoting EMT and decreasing the expression of genes such as E-cadherin and Kiss1.
         datePublished:2011-09-03T00:00:00Z
         dateModified:2011-09-03T00:00:00Z
         pageStart:73
         pageEnd:82
         sameAs:https://doi.org/10.1007/s12307-011-0087-2
         keywords:
            3T3L1 adipocytes
            B16BL6
            EMT
            Snai1
            Kiss1
            Cancer Research
            Oncology
            Immunology
            Cell Biology
            Biochemistry
            general
            Biomedicine
         image:
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs12307-011-0087-2/MediaObjects/12307_2011_87_Fig1_HTML.gif
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs12307-011-0087-2/MediaObjects/12307_2011_87_Fig2_HTML.gif
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs12307-011-0087-2/MediaObjects/12307_2011_87_Fig3_HTML.gif
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs12307-011-0087-2/MediaObjects/12307_2011_87_Fig4_HTML.gif
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs12307-011-0087-2/MediaObjects/12307_2011_87_Fig5_HTML.gif
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs12307-011-0087-2/MediaObjects/12307_2011_87_Fig6_HTML.gif
         isPartOf:
            name:Cancer Microenvironment
            issn:
               1875-2284
               1875-2292
            volumeNumber:5
            type:
               Periodical
               PublicationVolume
         publisher:
            name:Springer Netherlands
            logo:
               url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
               type:ImageObject
            type:Organization
         author:
               name:Kyoko Kushiro
               affiliation:
                     name:University of Texas at Austin
                     address:
                        name:Institute for Cellular and Molecular Biology, University of Texas at Austin, Austin, USA
                        type:PostalAddress
                     type:Organization
               type:Person
               name:Randy A. Chu
               affiliation:
                     name:University of Texas at Austin
                     address:
                        name:School of Biological Sciences, University of Texas at Austin, Austin, USA
                        type:PostalAddress
                     type:Organization
               type:Person
               name:Akanksha Verma
               affiliation:
                     name:University of Texas at Austin
                     address:
                        name:School of Biological Sciences, University of Texas at Austin, Austin, USA
                        type:PostalAddress
                     type:Organization
               type:Person
               name:Nomelí P. Núñez
               affiliation:
                     name:University of Texas at Austin
                     address:
                        name:Institute for Cellular and Molecular Biology, University of Texas at Austin, Austin, USA
                        type:PostalAddress
                     type:Organization
                     name:The University of Texas at Austin
                     address:
                        name:Department of Nutritional Sciences, The University of Texas at Austin, Austin, 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:Adipocytes Promote B16BL6 Melanoma Cell Invasion and the Epithelial-to-Mesenchymal Transition
      description:Metastatic melanoma is one of the most deadly and evasive types of cancer. On average, cancer patients with metastatic melanoma survive only 6–9 months after diagnosis. Epidemiological and animal studies suggest that obesity increases the metastatic ability of malignant melanoma, though the mechanism is not known. In the present studies, we assessed the ability of 3T3L1 adipocytes to modulate B16BL6 melanoma cell invasion and the Epithelial-to-Mesenchymal Transition (EMT). For this purpose, we induced the differentiation of 3T3L1 fibroblasts to adipocytes. Then, we collected the cell culture media from both fibroblasts and adipocytes and determined their effect on the invasive ability and EMT gene expression of B16BL6 melanoma cells. Results show that adipocyte media increased that ability of B16BL6 cells to invade. The higher invasive ability of B16BL6 melanoma cells was associated with increased expression of EMT genes such as Snai1, MMP9, Twist, and Vimentin. Additionally, the expression of the cell-to-cell adhesion protein E-cadherin and the metastasis suppressor gene Kiss1 were down-regulated in these B16BL6 cells. Also, adipocytes had high levels of the pro-inflammatory cytokine Interleukin 6 (IL-6). Treatment of B16BL6 cells with IL-6 elicited similar effects as the adipocyte media; IL-6 promoted the invasive ability of B16BL6 melanoma cells, increased the expression of Snai1, and decreased Kiss1 expression. IL-6 neutralization, however, did not have a visible effect on adipocyte media-induced invasion and snai1 staining. In summary, adipocytes may increase the invasive ability of B16BL6 melanoma cells by promoting EMT and decreasing the expression of genes such as E-cadherin and Kiss1.
      datePublished:2011-09-03T00:00:00Z
      dateModified:2011-09-03T00:00:00Z
      pageStart:73
      pageEnd:82
      sameAs:https://doi.org/10.1007/s12307-011-0087-2
      keywords:
         3T3L1 adipocytes
         B16BL6
         EMT
         Snai1
         Kiss1
         Cancer Research
         Oncology
         Immunology
         Cell Biology
         Biochemistry
         general
         Biomedicine
      image:
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs12307-011-0087-2/MediaObjects/12307_2011_87_Fig1_HTML.gif
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs12307-011-0087-2/MediaObjects/12307_2011_87_Fig2_HTML.gif
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs12307-011-0087-2/MediaObjects/12307_2011_87_Fig3_HTML.gif
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs12307-011-0087-2/MediaObjects/12307_2011_87_Fig4_HTML.gif
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs12307-011-0087-2/MediaObjects/12307_2011_87_Fig5_HTML.gif
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs12307-011-0087-2/MediaObjects/12307_2011_87_Fig6_HTML.gif
      isPartOf:
         name:Cancer Microenvironment
         issn:
            1875-2284
            1875-2292
         volumeNumber:5
         type:
            Periodical
            PublicationVolume
      publisher:
         name:Springer Netherlands
         logo:
            url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
            type:ImageObject
         type:Organization
      author:
            name:Kyoko Kushiro
            affiliation:
                  name:University of Texas at Austin
                  address:
                     name:Institute for Cellular and Molecular Biology, University of Texas at Austin, Austin, USA
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Randy A. Chu
            affiliation:
                  name:University of Texas at Austin
                  address:
                     name:School of Biological Sciences, University of Texas at Austin, Austin, USA
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Akanksha Verma
            affiliation:
                  name:University of Texas at Austin
                  address:
                     name:School of Biological Sciences, University of Texas at Austin, Austin, USA
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Nomelí P. Núñez
            affiliation:
                  name:University of Texas at Austin
                  address:
                     name:Institute for Cellular and Molecular Biology, University of Texas at Austin, Austin, USA
                     type:PostalAddress
                  type:Organization
                  name:The University of Texas at Austin
                  address:
                     name:Department of Nutritional Sciences, The University of Texas at Austin, Austin, USA
                     type:PostalAddress
                  type:Organization
            email:[email protected]
            type:Person
      isAccessibleForFree:
      hasPart:
         isAccessibleForFree:
         cssSelector:.main-content
         type:WebPageElement
["Periodical","PublicationVolume"]:
      name:Cancer Microenvironment
      issn:
         1875-2284
         1875-2292
      volumeNumber:5
Organization:
      name:Springer Netherlands
      logo:
         url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
         type:ImageObject
      name:University of Texas at Austin
      address:
         name:Institute for Cellular and Molecular Biology, University of Texas at Austin, Austin, USA
         type:PostalAddress
      name:University of Texas at Austin
      address:
         name:School of Biological Sciences, University of Texas at Austin, Austin, USA
         type:PostalAddress
      name:University of Texas at Austin
      address:
         name:School of Biological Sciences, University of Texas at Austin, Austin, USA
         type:PostalAddress
      name:University of Texas at Austin
      address:
         name:Institute for Cellular and Molecular Biology, University of Texas at Austin, Austin, USA
         type:PostalAddress
      name:The University of Texas at Austin
      address:
         name:Department of Nutritional Sciences, The University of Texas at Austin, Austin, USA
         type:PostalAddress
ImageObject:
      url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
Person:
      name:Kyoko Kushiro
      affiliation:
            name:University of Texas at Austin
            address:
               name:Institute for Cellular and Molecular Biology, University of Texas at Austin, Austin, USA
               type:PostalAddress
            type:Organization
      name:Randy A. Chu
      affiliation:
            name:University of Texas at Austin
            address:
               name:School of Biological Sciences, University of Texas at Austin, Austin, USA
               type:PostalAddress
            type:Organization
      name:Akanksha Verma
      affiliation:
            name:University of Texas at Austin
            address:
               name:School of Biological Sciences, University of Texas at Austin, Austin, USA
               type:PostalAddress
            type:Organization
      name:Nomelí P. Núñez
      affiliation:
            name:University of Texas at Austin
            address:
               name:Institute for Cellular and Molecular Biology, University of Texas at Austin, Austin, USA
               type:PostalAddress
            type:Organization
            name:The University of Texas at Austin
            address:
               name:Department of Nutritional Sciences, The University of Texas at Austin, Austin, USA
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Institute for Cellular and Molecular Biology, University of Texas at Austin, Austin, USA
      name:School of Biological Sciences, University of Texas at Austin, Austin, USA
      name:School of Biological Sciences, University of Texas at Austin, Austin, USA
      name:Institute for Cellular and Molecular Biology, University of Texas at Austin, Austin, USA
      name:Department of Nutritional Sciences, The University of Texas at Austin, Austin, USA
WebPageElement:
      isAccessibleForFree:
      cssSelector:.main-content

External Links {🔗}(147)

Analytics and Tracking {📊}

Google Tag Manager

Libraries {📚}

Clipboard.js
Pace
Prism.js

4.32s.

LINK . SPRINGER . COM {}