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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. Questions
  9. Schema
  10. External Links
  11. Analytics And Tracking
  12. Libraries
  13. CDN Services

We are analyzing https://link.springer.com/article/10.1007/s00262-020-02511-0.

Title:
LincRNA-p21 knockdown reversed tumor-associated macrophages function by promoting MDM2 to antagonize* p53 activation and alleviate breast cancer development | Cancer Immunology, Immunotherapy
Description:
Tumor-associated macrophages (TAMs) are important regulators of the complex interplay between immune system and breast cancer. TAMs fuel the cancer progression and metastasis by reprogramming their specific functional phenotype in cancer settings. Therefore, it is important to clarify the mechanisms of shaping specific functional phenotype of macrophages in tumor milieu. LncRNA profiles of TAMs were identified by LncRNA microarray. Flow cytometry was used to detect the surface markers of TAMs. The co-localization among lincRNA-p21, p53 and Mouse Double Minute 2 (MDM2) was identified by FISH probe and immunofluorescence. PyVT-MMTV and BALB/c mice were used for in vivo analysis. In the present work, we found that lincRNA-p21 significantly up-regulated in 4T1 educated macrophages. LincRNA-p21 knockdown facilitated macrophage polarization into pro-inflammatory M1 in tumor microenvironment, which might be caused by MDM2 eliciting proteasome-dependent degradation to p53 and activated NF-κB and STAT3 pathway. TAMs with lincRNA-p21 knockdown induced cancer cell apoptosis, inhibited tumor cell migration and invasion. In vivo, lincRNA-p21 knockdown macrophage adoptive transfer could alleviate breast cancer progression. Our results indicated that lincRNA-p21 was a key regulator of TAMs function in tumor milieu. Our data also shed a light on novel therapeutic targets of tumors characterized by monocytes/macrophages infiltration.
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.

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

We see no obvious way the site makes money.

Not all websites focus on profit; some are designed to educate, connect people, or share useful tools. People create websites for numerous reasons. And this could be one such example. Link.springer.com might have a hidden revenue stream, but it's not something we can detect.

Keywords {🔍}

pubmed, article, cancer, google, scholar, cas, central, breast, cell, macrophage, lincrnap, macrophages, tumor, tumorassociated, polarization, tams, rev, zhou, microenvironment, noncoding, immunol, jiangsu, knockdown, mdm, metastasis, access, long, rna, yang, privacy, cookies, function, content, research, tian, guo, pathway, nat, role, chen, wang, data, information, publish, search, activation, lining, zhaoliang, immune, progression,

Topics {✒️}

hif-1/akt/mtor/p70s6k pathway activating rage/nf-kappab pathway month download article/chapter macrophages-induced lncrna rp11-627g18 nf-kappab/stat3 pathway activation huaxi xu & zhaoliang su lincrna-p21 impacts prognosis breast cancer biology macrophage-directed cancer immunotherapy article cancer immunology full article pdf revealing protein-lncrna interaction lincrna-p21 significantly advanced breast tumors hypoxic tumor cells related subjects breast cancer statistics invasive breast cancer tam receptor signaling privacy choices/manage cookies rna-p21 induction 4t1 educated macrophages ovarian cancer metastasis reactive oxygen species central laboratory social development foundation specific functional phenotype article zhou activated nf-κb lincrna-p21 enhancing p53 activity stat3 pathway anti-cancer strategies article log antagonize p53 activation european economic area population-based study de vries ege van der vegt p300 act synergistically coupled histone modifications nanjing medical university zhaoliang su fang guo long noncoding rnas breast cancer additional information publisher' conditions privacy policy nf90-binding long macrophage cross-talk

Questions {❓}

  • Luo Z, Wang Q, Lau WB, Lau B, Xu L, Zhao L, Yang H, Feng M, Xuan Y, Yang Y, Lei L, Wang C, Yi T, Zhao X, Wei Y, Zhou S (2016) Tumor microenvironment: the culprit for ovarian cancer metastasis?
  • Qiu SQ, Waaijer SJH, Zwager MC, de Vries EGE, van der Vegt B, Schroder CP (2018) Tumor-associated macrophages in breast cancer: innocent bystander or important player?

Schema {🗺️}

WebPage:
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         headline:LincRNA-p21 knockdown reversed tumor-associated macrophages function by promoting MDM2 to antagonize* p53 activation and alleviate breast cancer development
         description:Tumor-associated macrophages (TAMs) are important regulators of the complex interplay between immune system and breast cancer. TAMs fuel the cancer progression and metastasis by reprogramming their specific functional phenotype in cancer settings. Therefore, it is important to clarify the mechanisms of shaping specific functional phenotype of macrophages in tumor milieu. LncRNA profiles of TAMs were identified by LncRNA microarray. Flow cytometry was used to detect the surface markers of TAMs. The co-localization among lincRNA-p21, p53 and Mouse Double Minute 2 (MDM2) was identified by FISH probe and immunofluorescence. PyVT-MMTV and BALB/c mice were used for in vivo analysis. In the present work, we found that lincRNA-p21 significantly up-regulated in 4T1 educated macrophages. LincRNA-p21 knockdown facilitated macrophage polarization into pro-inflammatory M1 in tumor microenvironment, which might be caused by MDM2 eliciting proteasome-dependent degradation to p53 and activated NF-κB and STAT3 pathway. TAMs with lincRNA-p21 knockdown induced cancer cell apoptosis, inhibited tumor cell migration and invasion. In vivo, lincRNA-p21 knockdown macrophage adoptive transfer could alleviate breast cancer progression. Our results indicated that lincRNA-p21 was a key regulator of TAMs function in tumor milieu. Our data also shed a light on novel therapeutic targets of tumors characterized by monocytes/macrophages infiltration.
         datePublished:2020-02-15T00:00:00Z
         dateModified:2020-02-15T00:00:00Z
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            Immunology
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      headline:LincRNA-p21 knockdown reversed tumor-associated macrophages function by promoting MDM2 to antagonize* p53 activation and alleviate breast cancer development
      description:Tumor-associated macrophages (TAMs) are important regulators of the complex interplay between immune system and breast cancer. TAMs fuel the cancer progression and metastasis by reprogramming their specific functional phenotype in cancer settings. Therefore, it is important to clarify the mechanisms of shaping specific functional phenotype of macrophages in tumor milieu. LncRNA profiles of TAMs were identified by LncRNA microarray. Flow cytometry was used to detect the surface markers of TAMs. The co-localization among lincRNA-p21, p53 and Mouse Double Minute 2 (MDM2) was identified by FISH probe and immunofluorescence. PyVT-MMTV and BALB/c mice were used for in vivo analysis. In the present work, we found that lincRNA-p21 significantly up-regulated in 4T1 educated macrophages. LincRNA-p21 knockdown facilitated macrophage polarization into pro-inflammatory M1 in tumor microenvironment, which might be caused by MDM2 eliciting proteasome-dependent degradation to p53 and activated NF-κB and STAT3 pathway. TAMs with lincRNA-p21 knockdown induced cancer cell apoptosis, inhibited tumor cell migration and invasion. In vivo, lincRNA-p21 knockdown macrophage adoptive transfer could alleviate breast cancer progression. Our results indicated that lincRNA-p21 was a key regulator of TAMs function in tumor milieu. Our data also shed a light on novel therapeutic targets of tumors characterized by monocytes/macrophages infiltration.
      datePublished:2020-02-15T00:00:00Z
      dateModified:2020-02-15T00:00:00Z
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         TAMs
         lincRNA-p21
         Breast cancer
         p53
         Tumor microenvironment
         Oncology
         Immunology
         Cancer Research
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                     type:PostalAddress
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                  address:
                     name:International Genome Center, Jiangsu University, Zhenjiang, China
                     type:PostalAddress
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            name:Fang Guo
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                  name:Changzhou Woman and Children Health Hospital Affiliated to Nanjing Medical University
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                     name:The Central Laboratory, Changzhou Woman and Children Health Hospital Affiliated to Nanjing Medical University, Changzhou, China
                     type:PostalAddress
                  type:Organization
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            name:Bin Yu
            affiliation:
                  name:Changzhou Woman and Children Health Hospital Affiliated to Nanjing Medical University
                  address:
                     name:The Central Laboratory, Changzhou Woman and Children Health Hospital Affiliated to Nanjing Medical University, Changzhou, China
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                  address:
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                     type:PostalAddress
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            name:Huaxi Xu
            affiliation:
                  name:Jiangsu University
                  address:
                     name:International Genome Center, Jiangsu University, Zhenjiang, China
                     type:PostalAddress
                  type:Organization
                  name:Jiangsu University
                  address:
                     name:Department of Immunology, Jiangsu University, Zhenjiang, China
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Zhaoliang Su
            url:http://orcid.org/0000-0002-5998-5575
            affiliation:
                  name:Jiangsu University
                  address:
                     name:International Genome Center, Jiangsu University, Zhenjiang, China
                     type:PostalAddress
                  type:Organization
                  name:Jiangsu University
                  address:
                     name:Department of Immunology, Jiangsu University, Zhenjiang, China
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      name:Cancer Immunology, Immunotherapy
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         name:The Central Laboratory, Changzhou Woman and Children Health Hospital Affiliated to Nanjing Medical University, Changzhou, China
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      name:Jiangsu University
      address:
         name:International Genome Center, Jiangsu University, Zhenjiang, China
         type:PostalAddress
      name:Jiangsu University
      address:
         name:Department of Immunology, Jiangsu University, Zhenjiang, China
         type:PostalAddress
      name:Jiangsu University
      address:
         name:International Genome Center, Jiangsu University, Zhenjiang, China
         type:PostalAddress
      name:Jiangsu University
      address:
         name:Department of Immunology, Jiangsu University, Zhenjiang, China
         type:PostalAddress
      name:Jiangsu University
      address:
         name:International Genome Center, Jiangsu University, Zhenjiang, China
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      name:Lining Zhou
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            name:Jiangsu University
            address:
               name:International Genome Center, Jiangsu University, Zhenjiang, China
               type:PostalAddress
            type:Organization
            name:Jiangsu University
            address:
               name:Department of Immunology, Jiangsu University, Zhenjiang, China
               type:PostalAddress
            type:Organization
      name:Yu Tian
      affiliation:
            name:Jiangsu University
            address:
               name:International Genome Center, Jiangsu University, Zhenjiang, China
               type:PostalAddress
            type:Organization
            name:Jiangsu University
            address:
               name:Department of Immunology, Jiangsu University, Zhenjiang, China
               type:PostalAddress
            type:Organization
      name:Fang Guo
      affiliation:
            name:Changzhou Woman and Children Health Hospital Affiliated to Nanjing Medical University
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               name:The Central Laboratory, Changzhou Woman and Children Health Hospital Affiliated to Nanjing Medical University, Changzhou, China
               type:PostalAddress
            type:Organization
      name:Bin Yu
      affiliation:
            name:Changzhou Woman and Children Health Hospital Affiliated to Nanjing Medical University
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               name:The Central Laboratory, Changzhou Woman and Children Health Hospital Affiliated to Nanjing Medical University, Changzhou, China
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            address:
               name:International Genome Center, Jiangsu University, Zhenjiang, China
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      affiliation:
            name:Jiangsu University
            address:
               name:International Genome Center, Jiangsu University, Zhenjiang, China
               type:PostalAddress
            type:Organization
            name:Jiangsu University
            address:
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      name:Zhaoliang Su
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            name:Jiangsu University
            address:
               name:International Genome Center, Jiangsu University, Zhenjiang, China
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            name:Jiangsu University
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      name:Department of Immunology, Jiangsu University, Zhenjiang, China
      name:International Genome Center, Jiangsu University, Zhenjiang, China
      name:Department of Immunology, Jiangsu University, Zhenjiang, China
      name:The Central Laboratory, Changzhou Woman and Children Health Hospital Affiliated to Nanjing Medical University, Changzhou, China
      name:The Central Laboratory, Changzhou Woman and Children Health Hospital Affiliated to Nanjing Medical University, Changzhou, China
      name:International Genome Center, Jiangsu University, Zhenjiang, China
      name:Department of Immunology, Jiangsu University, Zhenjiang, China
      name:International Genome Center, Jiangsu University, Zhenjiang, China
      name:Department of Immunology, Jiangsu University, Zhenjiang, China
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External Links {🔗}(228)

Analytics and Tracking {📊}

  • Google Tag Manager

Libraries {📚}

  • Clipboard.js
  • Prism.js

CDN Services {📦}

  • Crossref

4.12s.