We are analyzing https://link.springer.com/article/10.1007/s10620-013-2983-4.

Title:
Dysregulation of MicroRNA-34a Expression in Colorectal Cancer Inhibits the Phosphorylation of FAK Via VEGF | Digestive Diseases and Sciences
Description:
Background MicroRNAs (miRs) are small non-coding RNAs that play important roles in cancer development where they can act as oncogenes or as tumor-suppressors. MiR-34a is a tumor suppressor that is frequently downregulated in a number of tumor types. However, little is known about the role of miR-34a in colorectal cancer (CRC). Aim This study aims to show the dysregulation of miR-34a in CRC and to characterize the function and mechanism of miR-34a in CRC cell lines. Methods The expression of miR-34a was detected using real-time PCR on CRC tissues and adjacent non-tumorous tissues. The ELISA was used to assess vascular endothelial growth factor (VEGF). The focal adhesion kinase (FAK) and phosphorylated FAK Y397 (pY397FAK) were measured by Western blot. The functions of miR-34a in vivo were measured by migration, invasion, CCK-8 assay and flow cytometry. Results MiR-34a was significantly downregulated and pY397FAK was upregulated in CRC cancer tissues. It plays an important role in inhibiting migration and invasion and in increasing apoptosis of CRC cells. Bioinformatic analysis suggested that VEGF may be a target of miR-34a, and this hypothesis was proved by ELISA and RT-PCR. The level of pY397FAK that could be activated by VEGF was downregulated in miR-34a overexpression CRC cell lines. The phosphorylation of FAK at 397 sites in miR-34a-stable cell lines was completely rescued by extra VEGF treatment. Conclusion MiR-34a is frequently downregulated in CRC and modulates the phosphorylation of FAK by negatively regulating VEGF.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {📚}

Education
Health & Fitness
Science

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 5,000,019 visitors per month in the current month.
However, some sources were not loaded, we suggest to reload the page to get complete results.

check SE Ranking
check Ahrefs
check Similarweb
check Ubersuggest
check Semrush

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

We don’t know how the website earns money.

Some websites aren't about earning revenue; they're built to connect communities or raise awareness. There are numerous motivations behind creating websites. This might be one of them. Link.springer.com could have a money-making trick up its sleeve, but it's undetectable for now.

Keywords {🔍}

pubmed, cancer, article, google, scholar, cas, mira, cell, central, colorectal, expression, fak, vegf, cells, crc, tumor, wang, privacy, cookies, content, analysis, research, search, zhang, dong, kinase, access, mirna, microrna, publish, inhibits, phosphorylation, downregulated, focal, pyfak, pathway, targeting, human, breast, lung, oncol, res, data, information, log, journal, dysregulation, december, zhou, ming,

Topics {✒️}

month download article/chapter vegf-induced vascular permeability mir-34a-stable cell lines fak/rho gtpase activation jianping zhou & ming dong small-cell lung cancer hbv-positive hepatocellular carcinoma protein represses mirna-148a article digestive diseases human mir-34a microrna pre-mirna flanking region lygdi signaling pathway mir-34a enhances radiosensitivity full article pdf focal adhesion kinase colorectal cancer cells colorectal cancer progression related subjects colorectal cancer inhibits metastatic colorectal cancer human cancers privacy choices/manage cookies crc cell lines regulates cell motility colon cancer human glioblastoma cells colorectal cancer metastasis colorectal cancer patients inhibits tumor angiogenesis breast cancer risk cell struct funct dendritic cell differentiation microrna-34a expression mirna cancer therapeutics mir-200 microrna family germline microrna snps mir-34a inhibits results mir-34a conclusion mir-34a upregulating mir-34a bmc cancer negatively regulating vegf anti-vegf drugs mol biol cell cell growth targeting epigenetic regulation phosphorylated fak y397 european economic area drug discov today den boer ml

Schema {🗺️}

WebPage:
      mainEntity:
         headline:Dysregulation of MicroRNA-34a Expression in Colorectal Cancer Inhibits the Phosphorylation of FAK Via VEGF
         description:MicroRNAs (miRs) are small non-coding RNAs that play important roles in cancer development where they can act as oncogenes or as tumor-suppressors. MiR-34a is a tumor suppressor that is frequently downregulated in a number of tumor types. However, little is known about the role of miR-34a in colorectal cancer (CRC). This study aims to show the dysregulation of miR-34a in CRC and to characterize the function and mechanism of miR-34a in CRC cell lines. The expression of miR-34a was detected using real-time PCR on CRC tissues and adjacent non-tumorous tissues. The ELISA was used to assess vascular endothelial growth factor (VEGF). The focal adhesion kinase (FAK) and phosphorylated FAK Y397 (pY397FAK) were measured by Western blot. The functions of miR-34a in vivo were measured by migration, invasion, CCK-8 assay and flow cytometry. MiR-34a was significantly downregulated and pY397FAK was upregulated in CRC cancer tissues. It plays an important role in inhibiting migration and invasion and in increasing apoptosis of CRC cells. Bioinformatic analysis suggested that VEGF may be a target of miR-34a, and this hypothesis was proved by ELISA and RT-PCR. The level of pY397FAK that could be activated by VEGF was downregulated in miR-34a overexpression CRC cell lines. The phosphorylation of FAK at 397 sites in miR-34a-stable cell lines was completely rescued by extra VEGF treatment. MiR-34a is frequently downregulated in CRC and modulates the phosphorylation of FAK by negatively regulating VEGF.
         datePublished:2013-12-27T00:00:00Z
         dateModified:2013-12-27T00:00:00Z
         pageStart:958
         pageEnd:967
         sameAs:https://doi.org/10.1007/s10620-013-2983-4
         keywords:
            MiR-34a
            Colorectal cancer
            FAK
            pY397FAK
            VEGF
            Gastroenterology
            Hepatology
            Oncology
            Transplant Surgery
            Biochemistry
            general
         image:
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs10620-013-2983-4/MediaObjects/10620_2013_2983_Fig1_HTML.gif
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs10620-013-2983-4/MediaObjects/10620_2013_2983_Fig2_HTML.gif
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs10620-013-2983-4/MediaObjects/10620_2013_2983_Fig3_HTML.gif
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs10620-013-2983-4/MediaObjects/10620_2013_2983_Fig4_HTML.gif
         isPartOf:
            name:Digestive Diseases and Sciences
            issn:
               1573-2568
               0163-2116
            volumeNumber:59
            type:
               Periodical
               PublicationVolume
         publisher:
            name:Springer US
            logo:
               url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
               type:ImageObject
            type:Organization
         author:
               name:Danhua Zhang
               affiliation:
                     name:China Medical University
                     address:
                        name:Department of General Surgery, Gastrointestinal Surgery, The First Hospital, China Medical University, Shenyang, China
                        type:PostalAddress
                     type:Organization
               type:Person
               name:Jianping Zhou
               affiliation:
                     name:China Medical University
                     address:
                        name:Department of General Surgery, Gastrointestinal Surgery, The First Hospital, China Medical University, Shenyang, China
                        type:PostalAddress
                     type:Organization
               type:Person
               name:Ming Dong
               affiliation:
                     name:China Medical University
                     address:
                        name:Department of General Surgery, Gastrointestinal Surgery, The First Hospital, China Medical University, Shenyang, China
                        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:Dysregulation of MicroRNA-34a Expression in Colorectal Cancer Inhibits the Phosphorylation of FAK Via VEGF
      description:MicroRNAs (miRs) are small non-coding RNAs that play important roles in cancer development where they can act as oncogenes or as tumor-suppressors. MiR-34a is a tumor suppressor that is frequently downregulated in a number of tumor types. However, little is known about the role of miR-34a in colorectal cancer (CRC). This study aims to show the dysregulation of miR-34a in CRC and to characterize the function and mechanism of miR-34a in CRC cell lines. The expression of miR-34a was detected using real-time PCR on CRC tissues and adjacent non-tumorous tissues. The ELISA was used to assess vascular endothelial growth factor (VEGF). The focal adhesion kinase (FAK) and phosphorylated FAK Y397 (pY397FAK) were measured by Western blot. The functions of miR-34a in vivo were measured by migration, invasion, CCK-8 assay and flow cytometry. MiR-34a was significantly downregulated and pY397FAK was upregulated in CRC cancer tissues. It plays an important role in inhibiting migration and invasion and in increasing apoptosis of CRC cells. Bioinformatic analysis suggested that VEGF may be a target of miR-34a, and this hypothesis was proved by ELISA and RT-PCR. The level of pY397FAK that could be activated by VEGF was downregulated in miR-34a overexpression CRC cell lines. The phosphorylation of FAK at 397 sites in miR-34a-stable cell lines was completely rescued by extra VEGF treatment. MiR-34a is frequently downregulated in CRC and modulates the phosphorylation of FAK by negatively regulating VEGF.
      datePublished:2013-12-27T00:00:00Z
      dateModified:2013-12-27T00:00:00Z
      pageStart:958
      pageEnd:967
      sameAs:https://doi.org/10.1007/s10620-013-2983-4
      keywords:
         MiR-34a
         Colorectal cancer
         FAK
         pY397FAK
         VEGF
         Gastroenterology
         Hepatology
         Oncology
         Transplant Surgery
         Biochemistry
         general
      image:
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs10620-013-2983-4/MediaObjects/10620_2013_2983_Fig1_HTML.gif
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs10620-013-2983-4/MediaObjects/10620_2013_2983_Fig2_HTML.gif
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs10620-013-2983-4/MediaObjects/10620_2013_2983_Fig3_HTML.gif
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs10620-013-2983-4/MediaObjects/10620_2013_2983_Fig4_HTML.gif
      isPartOf:
         name:Digestive Diseases and Sciences
         issn:
            1573-2568
            0163-2116
         volumeNumber:59
         type:
            Periodical
            PublicationVolume
      publisher:
         name:Springer US
         logo:
            url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
            type:ImageObject
         type:Organization
      author:
            name:Danhua Zhang
            affiliation:
                  name:China Medical University
                  address:
                     name:Department of General Surgery, Gastrointestinal Surgery, The First Hospital, China Medical University, Shenyang, China
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Jianping Zhou
            affiliation:
                  name:China Medical University
                  address:
                     name:Department of General Surgery, Gastrointestinal Surgery, The First Hospital, China Medical University, Shenyang, China
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Ming Dong
            affiliation:
                  name:China Medical University
                  address:
                     name:Department of General Surgery, Gastrointestinal Surgery, The First Hospital, China Medical University, Shenyang, China
                     type:PostalAddress
                  type:Organization
            email:[email protected]
            type:Person
      isAccessibleForFree:
      hasPart:
         isAccessibleForFree:
         cssSelector:.main-content
         type:WebPageElement
["Periodical","PublicationVolume"]:
      name:Digestive Diseases and Sciences
      issn:
         1573-2568
         0163-2116
      volumeNumber:59
Organization:
      name:Springer US
      logo:
         url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
         type:ImageObject
      name:China Medical University
      address:
         name:Department of General Surgery, Gastrointestinal Surgery, The First Hospital, China Medical University, Shenyang, China
         type:PostalAddress
      name:China Medical University
      address:
         name:Department of General Surgery, Gastrointestinal Surgery, The First Hospital, China Medical University, Shenyang, China
         type:PostalAddress
      name:China Medical University
      address:
         name:Department of General Surgery, Gastrointestinal Surgery, The First Hospital, China Medical University, Shenyang, China
         type:PostalAddress
ImageObject:
      url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
Person:
      name:Danhua Zhang
      affiliation:
            name:China Medical University
            address:
               name:Department of General Surgery, Gastrointestinal Surgery, The First Hospital, China Medical University, Shenyang, China
               type:PostalAddress
            type:Organization
      name:Jianping Zhou
      affiliation:
            name:China Medical University
            address:
               name:Department of General Surgery, Gastrointestinal Surgery, The First Hospital, China Medical University, Shenyang, China
               type:PostalAddress
            type:Organization
      name:Ming Dong
      affiliation:
            name:China Medical University
            address:
               name:Department of General Surgery, Gastrointestinal Surgery, The First Hospital, China Medical University, Shenyang, China
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Department of General Surgery, Gastrointestinal Surgery, The First Hospital, China Medical University, Shenyang, China
      name:Department of General Surgery, Gastrointestinal Surgery, The First Hospital, China Medical University, Shenyang, China
      name:Department of General Surgery, Gastrointestinal Surgery, The First Hospital, China Medical University, Shenyang, China
WebPageElement:
      isAccessibleForFree:
      cssSelector:.main-content

External Links {🔗}(125)

Analytics and Tracking {📊}

Google Tag Manager

Libraries {📚}

Clipboard.js
Prism.js

CDN Services {📦}

Crossref

4.18s.

LINK . SPRINGER . COM {}