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LINK . SPRINGER . COM {}

  1. Analyzed Page
  2. Matching Content Categories
  3. CMS
  4. Monthly Traffic Estimate
  5. How Does Link.springer.com Make Money
  6. Keywords
  7. Topics
  8. Schema
  9. External Links
  10. Analytics And Tracking
  11. Libraries
  12. CDN Services

We are analyzing https://link.springer.com/article/10.1007/s13277-016-4964-7.

Title:
Regulation of proliferation, angiogenesis and apoptosis in hepatocellular carcinoma by miR-26b-5p | Tumor Biology
Description:
MicroRNAs (miRNAs) play vital roles in cell proliferation, differentiation and apoptosis in hepatocellular carcinoma (HCC). miR-26b has been confirmed as an important regulator in carcinogenesis and other pathological processes. miR-26b-5p is one member of the mature miR-26 family, and its functional role in proliferation, angiogenesis and apoptosis in HCC remains unknown. Here, we demonstrate that miR-26b-5p expression was significantly decreased in HCC tissues and HCC cell lines compared with normal liver tissues and liver cells by quantitative real-time polymerase chain reaction (qRT-PCR). The relationships between miR-26b-5p and the clinical characteristics of HCC patients were further analysed, and miR-26b-5p was positively correlated with the differentiation of HCC cells. Computational searches were further used to identify the downstream targets and signalling pathways of miR-26b-5p in HCC cells. Cell viability, proliferation and tube formation abilities were assessed by scrape, 3-(4,5 dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and three-dimensional culture assays to confirm that miR-26b-5p inhibited HCC cell growth and impaired the tube formation ability of the HCC cells. Both in vitro and in vivo studies showed that miR-26b-5p could suppress vascular mimicry (VM) and angiogenesis by down-regulating the expression of VE-cadherin, Snail and MMP2 and could inhibit the apoptosis of HCC cells. Using mouse models, we revealed that tumours derived from miR-26b-5p-expressing HCC cells displayed a significant decrease in microvessel density compared with those derived from control cells. Therefore, our data provide further insight into the role of miR-26b-5p as a negative regulator of proliferation, angiogenesis, and apoptosis in HCC.
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 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.

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

We see no obvious way the site makes money.

Earning money isn't the goal of every website; some are designed to offer support or promote social causes. People have different reasons for creating websites. This might be one such reason. Link.springer.com could be getting rich in stealth mode, or the way it's monetizing isn't detectable.

Keywords {🔍}

article, pubmed, google, scholar, cas, cancer, carcinoma, hepatocellular, tumor, cell, sun, apoptosis, wang, zhang, zhao, hcc, cells, mirbp, tianjin, liu, angiogenesis, expression, proliferation, liver, mimicry, targeting, microrna, micrornab, vasculogenic, baocun, central, biol, china, human, yang, regulating, transition, hepatology, doihep, privacy, cookies, content, data, fang, role, access, epithelialmesenchymal, invasion, mol, department,

Topics {✒️}

c-myc suppresses microrna-29b month download article/chapter real-time quantitative pcr epithelial-stromal cross-talk epithelial-mesenchymal transition mir-26b-5p expression suppress tumor growth targeting pi3k/akt pathway tumor angiogenic factor cutaneous malignant melanoma—implications human ovarian carcinoma—role full article pdf mir-26b-5p microrna-26b suppresses suppressing mir-29b mesenchymal transition privacy choices/manage cookies hubler jr wr hepatocellular carcinoma cells regulating cell cycle human liver cancers downregulating jun expression downregulating rock1 expression mature mir-26 family related subjects cell cycle progression human melanoma cells article wang mir-1285-3p acts tube formation abilities tube formation ability microvessel density compared promote drug resistance promote tumor aggressiveness high tumor grade mol cancer ther human skin tumors mol cell biol human breast cancer cancer biol ther vascular channel formation hcc remains unknown huaier suppresses proliferation european economic area dimensional culture assays agosto-perez fj ethics declarations conflicts electronic supplementary material tumor cell metastasis bmc cancer

Schema {🗺️}

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         headline:Regulation of proliferation, angiogenesis and apoptosis in hepatocellular carcinoma by miR-26b-5p
         description:MicroRNAs (miRNAs) play vital roles in cell proliferation, differentiation and apoptosis in hepatocellular carcinoma (HCC). miR-26b has been confirmed as an important regulator in carcinogenesis and other pathological processes. miR-26b-5p is one member of the mature miR-26 family, and its functional role in proliferation, angiogenesis and apoptosis in HCC remains unknown. Here, we demonstrate that miR-26b-5p expression was significantly decreased in HCC tissues and HCC cell lines compared with normal liver tissues and liver cells by quantitative real-time polymerase chain reaction (qRT-PCR). The relationships between miR-26b-5p and the clinical characteristics of HCC patients were further analysed, and miR-26b-5p was positively correlated with the differentiation of HCC cells. Computational searches were further used to identify the downstream targets and signalling pathways of miR-26b-5p in HCC cells. Cell viability, proliferation and tube formation abilities were assessed by scrape, 3-(4,5 dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and three-dimensional culture assays to confirm that miR-26b-5p inhibited HCC cell growth and impaired the tube formation ability of the HCC cells. Both in vitro and in vivo studies showed that miR-26b-5p could suppress vascular mimicry (VM) and angiogenesis by down-regulating the expression of VE-cadherin, Snail and MMP2 and could inhibit the apoptosis of HCC cells. Using mouse models, we revealed that tumours derived from miR-26b-5p-expressing HCC cells displayed a significant decrease in microvessel density compared with those derived from control cells. Therefore, our data provide further insight into the role of miR-26b-5p as a negative regulator of proliferation, angiogenesis, and apoptosis in HCC.
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            Apoptosis
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            Cancer Research
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      headline:Regulation of proliferation, angiogenesis and apoptosis in hepatocellular carcinoma by miR-26b-5p
      description:MicroRNAs (miRNAs) play vital roles in cell proliferation, differentiation and apoptosis in hepatocellular carcinoma (HCC). miR-26b has been confirmed as an important regulator in carcinogenesis and other pathological processes. miR-26b-5p is one member of the mature miR-26 family, and its functional role in proliferation, angiogenesis and apoptosis in HCC remains unknown. Here, we demonstrate that miR-26b-5p expression was significantly decreased in HCC tissues and HCC cell lines compared with normal liver tissues and liver cells by quantitative real-time polymerase chain reaction (qRT-PCR). The relationships between miR-26b-5p and the clinical characteristics of HCC patients were further analysed, and miR-26b-5p was positively correlated with the differentiation of HCC cells. Computational searches were further used to identify the downstream targets and signalling pathways of miR-26b-5p in HCC cells. Cell viability, proliferation and tube formation abilities were assessed by scrape, 3-(4,5 dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and three-dimensional culture assays to confirm that miR-26b-5p inhibited HCC cell growth and impaired the tube formation ability of the HCC cells. Both in vitro and in vivo studies showed that miR-26b-5p could suppress vascular mimicry (VM) and angiogenesis by down-regulating the expression of VE-cadherin, Snail and MMP2 and could inhibit the apoptosis of HCC cells. Using mouse models, we revealed that tumours derived from miR-26b-5p-expressing HCC cells displayed a significant decrease in microvessel density compared with those derived from control cells. Therefore, our data provide further insight into the role of miR-26b-5p as a negative regulator of proliferation, angiogenesis, and apoptosis in HCC.
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         miR-26b-5p
         Angiogenesis
         Apoptosis
         Hepatocellular carcinoma
         Cancer Research
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               type:PostalAddress
            type:Organization
      name:Xiulan Zhao
      affiliation:
            name:Tianjin Medical University
            address:
               name:Department of Pathology, Tianjin Medical University, Tianjin, China
               type:PostalAddress
            type:Organization
            name:Tianjin Medical University
            address:
               name:Department of Pathology, Tianjin General Hospital, Tianjin Medical University, Tianjin, China
               type:PostalAddress
            type:Organization
      name:Xudong Wang
      affiliation:
            name:Tianjin Medical University
            address:
               name:Department of Pathology, Tianjin Cancer Hospital, Tianjin Medical University, Tianjin, China
               type:PostalAddress
            type:Organization
      name:Nan Zhao
      affiliation:
            name:Tianjin Medical University
            address:
               name:Department of Pathology, Tianjin Medical University, Tianjin, China
               type:PostalAddress
            type:Organization
      name:Yanhui Zhang
      affiliation:
            name:Tianjin Medical University
            address:
               name:Department of Pathology, Tianjin Cancer Hospital, Tianjin Medical University, Tianjin, China
               type:PostalAddress
            type:Organization
      name:Yanlei Li
      affiliation:
            name:Tianjin Medical University
            address:
               name:Department of Pathology, Tianjin Medical University, Tianjin, China
               type:PostalAddress
            type:Organization
      name:Qiang Gu
      affiliation:
            name:Tianjin Medical University
            address:
               name:Department of Pathology, Tianjin Medical University, Tianjin, China
               type:PostalAddress
            type:Organization
            name:Tianjin Medical University
            address:
               name:Department of Pathology, Tianjin General Hospital, Tianjin Medical University, Tianjin, China
               type:PostalAddress
            type:Organization
      name:Fang Liu
      affiliation:
            name:Tianjin Medical University
            address:
               name:Department of Pathology, Tianjin Medical University, Tianjin, China
               type:PostalAddress
            type:Organization
            name:Tianjin Medical University
            address:
               name:Department of Pathology, Tianjin General Hospital, Tianjin Medical University, Tianjin, China
               type:PostalAddress
            type:Organization
      name:Bing Shao
      affiliation:
            name:Tianjin Medical University
            address:
               name:Department of Pathology, Tianjin Medical University, Tianjin, China
               type:PostalAddress
            type:Organization
      name:Jindan An
      affiliation:
            name:Mudanjiang Medical University
            address:
               name:Department of Pathology, Mudanjiang Medical University, Heilongjiang, China
               type:PostalAddress
            type:Organization
PostalAddress:
      name:Department of Pathology, Tianjin Medical University, Tianjin, China
      name:Department of Pathology, Tianjin Medical University, Tianjin, China
      name:Department of Pathology, Tianjin Cancer Hospital, Tianjin Medical University, Tianjin, China
      name:Department of Pathology, Tianjin General Hospital, Tianjin Medical University, Tianjin, China
      name:Department of Pathology and Cancer Hospital and General Hospital of Tianjin, Medical University, Tianjin, China
      name:Department of Pathology, Tianjin Medical University, Tianjin, China
      name:Department of Pathology, Tianjin Medical University, Tianjin, China
      name:Department of Pathology, Tianjin General Hospital, Tianjin Medical University, Tianjin, China
      name:Department of Pathology, Tianjin Cancer Hospital, Tianjin Medical University, Tianjin, China
      name:Department of Pathology, Tianjin Medical University, Tianjin, China
      name:Department of Pathology, Tianjin Cancer Hospital, Tianjin Medical University, Tianjin, China
      name:Department of Pathology, Tianjin Medical University, Tianjin, China
      name:Department of Pathology, Tianjin Medical University, Tianjin, China
      name:Department of Pathology, Tianjin General Hospital, Tianjin Medical University, Tianjin, China
      name:Department of Pathology, Tianjin Medical University, Tianjin, China
      name:Department of Pathology, Tianjin General Hospital, Tianjin Medical University, Tianjin, China
      name:Department of Pathology, Tianjin Medical University, Tianjin, China
      name:Department of Pathology, Mudanjiang Medical University, Heilongjiang, China
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