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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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  13. CDN Services

We are analyzing https://link.springer.com/article/10.1186/s13046-018-0726-2.

Title:
Radiotherapy-induced cell death activates paracrine HMGB1-TLR2 signaling and accelerates pancreatic carcinoma metastasis | Journal of Experimental & Clinical Cancer Research
Description:
Background Dying cells after irradiation could promote the repopulation of surviving cancer cells leading to tumor recurrence. We aim to define the role of dying cells in promoting pancreatic cancer cells metastasis following radiotherapy. Methods Using the transwell system as the in vitro co-culture model, a small number of untreated pancreatic cancer cells were seeded in the upper chamber, while a larger number of lethally treated pancreatic cancer cells were seeded in the lower chamber. A series of experiments were conducted to investigate the role of dying-cell-derived HMGB1 on the invasion of pancreatic cancer in vitro and cancer metastasis in vivo. We then designed shRNA knockdown and Western blot assays to detect signaling activity. Results We found that dying pancreatic cancer cells significantly promote the invasion of pancreatic cancer cells in vitro and cancer metastasis in vivo. HMGB1 gene knockdown attenuated the migration-stimulating effect of irradiated, dying cells on living pancreatic cancer cells. Finally, we showed that dying-cell-derived HMGB1 functions in a paracrine manner to affect cancer-cell migration dependent on acquiring an epithelial-mesenchymal transition (EMT) phenotype and PI3K/pAkt activation. This process is mediated by the receptor for TLR2. Conclusion Our study indicates that, during radiotherapy, dying pancreatic cancer cells activate paracrine signaling events that promote the mobility of surviving tumor cells. We suggest a strategy to inhibit HMGB1 for preventing pancreatic carcinoma relapse and metastasis.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {📚}

  • Science
  • Health & Fitness
  • Education

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 8,170,536 visitors per month in the current month.

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

The income method remains a mystery to us.

Websites don't always need to be profitable; some serve as platforms for education or personal expression. Websites can serve multiple purposes. And this might be one of them. Link.springer.com has a secret sauce for making money, but we can't detect it yet.

Keywords {🔍}

cells, cancer, hmgb, pancreatic, cell, metastasis, pubmed, article, panc, tumor, google, scholar, fig, radiotherapy, cas, invasion, dying, carcinoma, signaling, irradiation, emt, group, ngml, expression, results, tlr, human, vitro, rhhmgb, caspase, control, data, treated, zhang, migration, central, research, death, hmgbs, analysis, vivo, zeb, promote, role, released, medium, level, groups, wang, transwell,

Topics {✒️}

dying-cell-derived hmgb1 activates erk/nf-kappab pathway hmgb1/tlr2 stimulates phosphorylation radiotherapy-induced hmgb1-tlr2 signaling promoting pancreatic-cancer-cell invasion dying-cell-derived hmgb1 plays dying-cell-derived hmgb1 functions tgf-beta signaling pathway hmgb1-/-panc-1 cell-derived supernatant pi3k/pakt-emt signaling axis dying-cell-derived hmgb1 dying-cell derived hmgb1 dying cell-derived hmgb1 dying cancer-cell marker varied-dose x-ray-treated article download pdf suppress t-cell responses pancreatic-cancer stem cells dongqing wang & haitao zhu ccl21/ccr7 axis contributed pi3k/akt signaling pathway pi3k/akt signaling pathways advanced-pancreatic-cancer patients soft-tissue density nodules emt-related transcriptional factors multiple context-dependent signals pi3k/akt/emt signaling high-mobility group box 1 hmgb1-mediated cell invasion avoid pancreatic-carcinoma relapse cohort=tcga%20pancreatic%20cancer%20 immunogenic cell death pancreatic-carcinoma tnm staging initial pro-metastasis factor emt-related transcription factors dying fibroblast cells radiated feeder-cells groups cell signaling technology cancer-cell cultured medium full size image stable cell lines hmgb1-mediated tlr2 signalling mediating cell invasion tumor cell repopulation tlr2/pi3k/akt pathways human fibroblast cells hmgb1–rage axis contributes randomly-selected microscopic fields lentivirus carrying hmgb1-shrna real-time quantitative pcr

Questions {❓}

  • High-mobility group protein 1(Y): metastasis-associated or metastasis-inducing?
  • Paradoxical role of HMGB1 in pancreatic cancer: tumor suppressor or tumor promoter?
  • Net/datapages/?

Schema {🗺️}

WebPage:
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         headline:Radiotherapy-induced cell death activates paracrine HMGB1-TLR2 signaling and accelerates pancreatic carcinoma metastasis
         description:Dying cells after irradiation could promote the repopulation of surviving cancer cells leading to tumor recurrence. We aim to define the role of dying cells in promoting pancreatic cancer cells metastasis following radiotherapy. Using the transwell system as the in vitro co-culture model, a small number of untreated pancreatic cancer cells were seeded in the upper chamber, while a larger number of lethally treated pancreatic cancer cells were seeded in the lower chamber. A series of experiments were conducted to investigate the role of dying-cell-derived HMGB1 on the invasion of pancreatic cancer in vitro and cancer metastasis in vivo. We then designed shRNA knockdown and Western blot assays to detect signaling activity. We found that dying pancreatic cancer cells significantly promote the invasion of pancreatic cancer cells in vitro and cancer metastasis in vivo. HMGB1 gene knockdown attenuated the migration-stimulating effect of irradiated, dying cells on living pancreatic cancer cells. Finally, we showed that dying-cell-derived HMGB1 functions in a paracrine manner to affect cancer-cell migration dependent on acquiring an epithelial-mesenchymal transition (EMT) phenotype and PI3K/pAkt activation. This process is mediated by the receptor for TLR2. Our study indicates that, during radiotherapy, dying pancreatic cancer cells activate paracrine signaling events that promote the mobility of surviving tumor cells. We suggest a strategy to inhibit HMGB1 for preventing pancreatic carcinoma relapse and metastasis.
         datePublished:2018-04-03T00:00:00Z
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            Metastasis
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            Cancer Research
            Immunology
            Apoptosis
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      headline:Radiotherapy-induced cell death activates paracrine HMGB1-TLR2 signaling and accelerates pancreatic carcinoma metastasis
      description:Dying cells after irradiation could promote the repopulation of surviving cancer cells leading to tumor recurrence. We aim to define the role of dying cells in promoting pancreatic cancer cells metastasis following radiotherapy. Using the transwell system as the in vitro co-culture model, a small number of untreated pancreatic cancer cells were seeded in the upper chamber, while a larger number of lethally treated pancreatic cancer cells were seeded in the lower chamber. A series of experiments were conducted to investigate the role of dying-cell-derived HMGB1 on the invasion of pancreatic cancer in vitro and cancer metastasis in vivo. We then designed shRNA knockdown and Western blot assays to detect signaling activity. We found that dying pancreatic cancer cells significantly promote the invasion of pancreatic cancer cells in vitro and cancer metastasis in vivo. HMGB1 gene knockdown attenuated the migration-stimulating effect of irradiated, dying cells on living pancreatic cancer cells. Finally, we showed that dying-cell-derived HMGB1 functions in a paracrine manner to affect cancer-cell migration dependent on acquiring an epithelial-mesenchymal transition (EMT) phenotype and PI3K/pAkt activation. This process is mediated by the receptor for TLR2. Our study indicates that, during radiotherapy, dying pancreatic cancer cells activate paracrine signaling events that promote the mobility of surviving tumor cells. We suggest a strategy to inhibit HMGB1 for preventing pancreatic carcinoma relapse and metastasis.
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      dateModified:2018-04-03T00:00:00Z
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         Pancreatic carcinoma
         HMGB1
         Metastasis
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         Cancer Research
         Immunology
         Apoptosis
         Oncology
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                     name:The Affiliated Hospital of Jiangsu University, Zhenjiang, China
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                     name:The Affiliated Hospital of Jiangsu University, Zhenjiang, China
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                  name:The Affiliated Hospital of Jiangsu University, Jiangsu University
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            name:The Affiliated Hospital of Jiangsu University, Jiangsu University
            address:
               name:Department of Radiology, The Affiliated Hospital of Jiangsu University, Jiangsu University, Zhenjiang, China
               type:PostalAddress
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      email:[email protected]
      name:Haitao Zhu
      affiliation:
            name:The Affiliated Hospital of Jiangsu University
            address:
               name:The Affiliated Hospital of Jiangsu University, Zhenjiang, China
               type:PostalAddress
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            name:The Affiliated Hospital of Jiangsu University, Jiangsu University
            address:
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      name:The Affiliated Hospital of Jiangsu University, Zhenjiang, China
      name:The First People’s Hospital of Zhenjiang, Zhenjiang, China
      name:Faculty of Science and Engineering, Åbo Akademi University and Turku Centre for Biotechnology, Turku, Finland
      name:The Affiliated Hospital of Jiangsu University, Zhenjiang, China
      name:The Affiliated Hospital of Jiangsu University, Zhenjiang, China
      name:School of Medicine, Jiangsu University, Zhenjiang, China
      name:The Affiliated Hospital of Jiangsu University, Zhenjiang, China
      name:Department of Radiology, The Affiliated Hospital of Jiangsu University, Jiangsu University, Zhenjiang, China
      name:The Affiliated Hospital of Jiangsu University, Zhenjiang, China
      name:Department of Radiology, The Affiliated Hospital of Jiangsu University, Jiangsu University, Zhenjiang, China

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