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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
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We are analyzing https://link.springer.com/article/10.1007/s10495-016-1214-9.

Title:
Enhanced autophagy reveals vulnerability of P-gp mediated epirubicin resistance in triple negative breast cancer cells | Apoptosis
Description:
Epirubicin (EPI) is widely used for triple negative breast cancer (TNBC), but a substantial number of patients develop EPI resistance that is associated with poor outcome. The underlying mechanism for EPI resistance remains poorly understood. We have developed and characterized an EPI-resistant (EPI-R) cell line from parental MDA-MB-231 cells. These EPI-R cells reached stable growth in the medium containing 8 μg/ml of EPI. They overexpressed P-glycoprotein (P-gp) and contained numerous autophagic vacuoles. The suppression of P-gp overexpression and/or autophagy restored the sensitivity of these EPI-R cells to EPI. We further show that autophagy conferred resistance to EPI on MDA cells by blocking the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB)-mediated pro-apoptotic signals. Together, these results reveal a synergistic role of P-gp, autophagy, and NF-κB pathways in the development of EPI resistance in TNBC cells. They also suggest that blocking the P-gp overexpression and autophagy may be an effective means of reducing EPI resistance.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {📚}

  • Science
  • Education
  • Health & Fitness

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 7,734,772 visitors per month in the current month.

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

We don’t know how the website earns money.

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 could have a money-making trick up its sleeve, but it's undetectable for now.

Keywords {🔍}

pubmed, article, google, scholar, cancer, cas, autophagy, cell, cells, resistance, breast, central, pgp, wang, apoptosis, zhang, epi, min, line, nfκb, research, res, epirubicin, triple, negative, yang, liu, role, triplenegative, china, oncol, lanzhou, privacy, cookies, content, chen, pglycoprotein, development, access, gansu, university, publish, search, xie, dong, epir, mdamb, autophagic, death, drug,

Topics {✒️}

nuclear factor kappa-light-chain-enhancer nf-κb-dependent trail resistance beta-catenin/gsk-3beta modulation triple-negative breast cancer targeting nuclear factor-kappa increases pgp-mediated multidrug-resistance month download article/chapter nf-κb activity decreases mda-mb-231/epi cell line nf-κb signaling pathways cisplatin-resistant cell line parental mda-mb-231 cells mediated pro-apoptotic signals er stress-induced autophagy k562/a02 cell line doxorubicin-treated mcf-7 cells anti-malaria drug artesunate bortezomib-induced cell death cell-cycle-dependent turnover nf-κb pathways facilitates epirubicin-resistance development breast cancer resistance abc-cassette transporters mitochondrial apoptosis pathway gastric cancer cells full article pdf metastatic breast cancer related subjects epirubicin-induced apoptosis multidrug-resistant cells article apoptosis aims pancreatic cancer cells nf-κb monitoring autophagic flux innovative research team fundamental research funds privacy choices/manage cookies mdr-1/p-gp autophagic cell death reis-filho js autophagy conferred resistance p-gp overexpression laffitte m-cn mtagrfp-mwasabi-lc3 breast cancer nme2 reduces proliferation stimuli-dependent fashion li s article zhang reducing epi resistance

Questions {❓}

  • Levine B, Yuan J (2005) Autophagy in cell death: an innocent convict?

Schema {🗺️}

WebPage:
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         headline:Enhanced autophagy reveals vulnerability of P-gp mediated epirubicin resistance in triple negative breast cancer cells
         description:Epirubicin (EPI) is widely used for triple negative breast cancer (TNBC), but a substantial number of patients develop EPI resistance that is associated with poor outcome. The underlying mechanism for EPI resistance remains poorly understood. We have developed and characterized an EPI-resistant (EPI-R) cell line from parental MDA-MB-231 cells. These EPI-R cells reached stable growth in the medium containing 8 μg/ml of EPI. They overexpressed P-glycoprotein (P-gp) and contained numerous autophagic vacuoles. The suppression of P-gp overexpression and/or autophagy restored the sensitivity of these EPI-R cells to EPI. We further show that autophagy conferred resistance to EPI on MDA cells by blocking the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB)-mediated pro-apoptotic signals. Together, these results reveal a synergistic role of P-gp, autophagy, and NF-κB pathways in the development of EPI resistance in TNBC cells. They also suggest that blocking the P-gp overexpression and autophagy may be an effective means of reducing EPI resistance.
         datePublished:2016-01-14T00:00:00Z
         dateModified:2016-01-14T00:00:00Z
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            P-gp
            NF-κB
            Epirubicin
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            Cancer Research
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            Oncology
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            general
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      headline:Enhanced autophagy reveals vulnerability of P-gp mediated epirubicin resistance in triple negative breast cancer cells
      description:Epirubicin (EPI) is widely used for triple negative breast cancer (TNBC), but a substantial number of patients develop EPI resistance that is associated with poor outcome. The underlying mechanism for EPI resistance remains poorly understood. We have developed and characterized an EPI-resistant (EPI-R) cell line from parental MDA-MB-231 cells. These EPI-R cells reached stable growth in the medium containing 8 μg/ml of EPI. They overexpressed P-glycoprotein (P-gp) and contained numerous autophagic vacuoles. The suppression of P-gp overexpression and/or autophagy restored the sensitivity of these EPI-R cells to EPI. We further show that autophagy conferred resistance to EPI on MDA cells by blocking the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB)-mediated pro-apoptotic signals. Together, these results reveal a synergistic role of P-gp, autophagy, and NF-κB pathways in the development of EPI resistance in TNBC cells. They also suggest that blocking the P-gp overexpression and autophagy may be an effective means of reducing EPI resistance.
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         Autophagy
         P-gp
         NF-κB
         Epirubicin
         Chemotherapy resistance
         Triple negative breast cancer
         Cancer Research
         Cell Biology
         Oncology
         Biochemistry
         general
         Virology
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      address:
         name:Institute of Pathology, School of Basic Medical Sciences, Lanzhou University, Lanzhou, China
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         name:Institute of Pathology, School of Basic Medical Sciences, Lanzhou University, Lanzhou, China
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      name:Ai-jun Yang
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      name:Min Wang
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            name:Lanzhou University
            address:
               name:Key Laboratory of Preclinical Study for New Drugs of Gansu Province, Lanzhou University, Lanzhou, China
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Institute of Integrated Traditional Chinese and Western Medicine, School of Basic Medical Sciences, Lanzhou University, Lanzhou, China
      name:Institute of Pathology, School of Basic Medical Sciences, Lanzhou University, Lanzhou, China
      name:Institute of Integrated Traditional Chinese and Western Medicine, School of Basic Medical Sciences, Lanzhou University, Lanzhou, China
      name:Institute of Pathology, School of Basic Medical Sciences, Lanzhou University, Lanzhou, China
      name:Institute of Integrated Traditional Chinese and Western Medicine, School of Basic Medical Sciences, Lanzhou University, Lanzhou, China
      name:Institute of Pathology, School of Basic Medical Sciences, Lanzhou University, Lanzhou, China
      name:Institute of Pathology, School of Basic Medical Sciences, Lanzhou University, Lanzhou, China
      name:Institute of Pathology, School of Basic Medical Sciences, Lanzhou University, Lanzhou, China
      name:Institute of Pathology, School of Basic Medical Sciences, Lanzhou University, Lanzhou, China
      name:Institute of Pathology, School of Basic Medical Sciences, Lanzhou University, Lanzhou, China
      name:BloodWorks Northwest Research Institute, Seattle, USA
      name:Division of Hematology, Department of Medicine, University of Washington, School of Medicine, Seattle, USA
      name:Institute of Integrated Traditional Chinese and Western Medicine, School of Basic Medical Sciences, Lanzhou University, Lanzhou, China
      name:Institute of Pathology, School of Basic Medical Sciences, Lanzhou University, Lanzhou, China
      name:Key Laboratory of Preclinical Study for New Drugs of Gansu Province, Lanzhou University, Lanzhou, China
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