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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
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We are analyzing https://link.springer.com/article/10.1007/s11357-017-9970-1.

Title:
Apigenin suppresses the senescence-associated secretory phenotype and paracrine effects on breast cancer cells | GeroScience
Description:
Apigenin (4′,5,7,-trihydroxyflavone) is a flavonoid found in certain herbs, fruits, and vegetables. Apigenin can attenuate inflammation, which is associated with many chronic diseases of aging. Senescent cells—stressed cells that accumulate with age in mammals—display a pro-inflammatory senescence-associated secretory phenotype (SASP) that can drive or exacerbate several age-related pathologies, including cancer. Flavonoids, including apigenin, were recently shown to reduce the SASP of a human fibroblast strain induced to senesce by bleomycin. Here, we confirm that apigenin suppresses the SASP in three human fibroblast strains induced to senesce by ionizing radiation, constitutive MAPK (mitogen-activated protein kinase) signaling, oncogenic RAS, or replicative exhaustion. Apigenin suppressed the SASP in part by suppressing IL-1α signaling through IRAK1 and IRAK4, p38-MAPK, and NF-κB. Apigenin was particularly potent at suppressing the expression and secretion of CXCL10 (IP10), a newly identified SASP factor. Further, apigenin-mediated suppression of the SASP substantially reduced the aggressive phenotype of human breast cancer cells, as determined by cell proliferation, extracellular matrix invasion, and epithelial-mesenchymal transition. Our results support the idea that apigenin is a promising natural product for reducing the impact of senescent cells on age-related diseases such as cancer.
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.
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How Does Link.springer.com Make Money? {💸}

We can't see how the site brings in money.

The purpose of some websites isn't monetary gain; they're meant to inform, educate, or foster collaboration. Everyone has unique reasons for building websites. This could be an example. Link.springer.com might be making money, but it's not detectable how they're doing it.

Keywords {🔍}

pubmed, article, google, scholar, cas, apigenin, cells, campisi, cell, central, senescenceassociated, senescent, cancer, secretory, flavonoids, phenotype, desprez, sasp, human, fibroblasts, aging, levels, research, inflammation, induced, expression, secretion, suppression, senescence, nature, biol, pdf, privacy, cookies, content, effects, senesce, nfκb, related, cellular, patil, freund, inflammatory, publish, search, geroscience, suppresses, breast, judith, access,

Topics {✒️}

mitogen-activated protein kinase phosphatidylinositol 3-kinase/akt-dependent pathway month download article/chapter nf-κb reporter activation nf-κb activation pathways extracellular matrix invasion il6/il-8 cytokine network epithelial-mesenchymal transition induced cell surface il-1α inactivating nf-kappab proinflammatory nf-kappab senescent cells—stressed cells p53 tumor suppressor recombinant il-1a remi-martin laberge article geroscience aims suppressing il-1α signaling hif-1α protein full article pdf sens research foundation human cellular senescence breast cancer cells cell proliferation privacy choices/manage cookies epithelial-mesenchymal transition matrix-degrading proteases mouse cells dependent dmso-treated ns cells nf-κb selective growth-inhibitory il-1a nf-kb p65 apigenin inhibits release decreasing caspase-3 activation coppé jp structurally related flavonoids age-related pathologies cell-cycle deregulatory cell cycle progression inflammatory cytokine secretion senescent hca2 cells secretory phenotype formation switches immune response cancer cell apoptosis anti-inflammatory activity senescent bj fibroblasts european economic area casaclang versoza gc van deursen jm pereira-smith om

Schema {🗺️}

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         headline:Apigenin suppresses the senescence-associated secretory phenotype and paracrine effects on breast cancer cells
         description:Apigenin (4′,5,7,-trihydroxyflavone) is a flavonoid found in certain herbs, fruits, and vegetables. Apigenin can attenuate inflammation, which is associated with many chronic diseases of aging. Senescent cells—stressed cells that accumulate with age in mammals—display a pro-inflammatory senescence-associated secretory phenotype (SASP) that can drive or exacerbate several age-related pathologies, including cancer. Flavonoids, including apigenin, were recently shown to reduce the SASP of a human fibroblast strain induced to senesce by bleomycin. Here, we confirm that apigenin suppresses the SASP in three human fibroblast strains induced to senesce by ionizing radiation, constitutive MAPK (mitogen-activated protein kinase) signaling, oncogenic RAS, or replicative exhaustion. Apigenin suppressed the SASP in part by suppressing IL-1α signaling through IRAK1 and IRAK4, p38-MAPK, and NF-κB. Apigenin was particularly potent at suppressing the expression and secretion of CXCL10 (IP10), a newly identified SASP factor. Further, apigenin-mediated suppression of the SASP substantially reduced the aggressive phenotype of human breast cancer cells, as determined by cell proliferation, extracellular matrix invasion, and epithelial-mesenchymal transition. Our results support the idea that apigenin is a promising natural product for reducing the impact of senescent cells on age-related diseases such as cancer.
         datePublished:2017-04-04T00:00:00Z
         dateModified:2017-04-04T00:00:00Z
         pageStart:161
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      headline:Apigenin suppresses the senescence-associated secretory phenotype and paracrine effects on breast cancer cells
      description:Apigenin (4′,5,7,-trihydroxyflavone) is a flavonoid found in certain herbs, fruits, and vegetables. Apigenin can attenuate inflammation, which is associated with many chronic diseases of aging. Senescent cells—stressed cells that accumulate with age in mammals—display a pro-inflammatory senescence-associated secretory phenotype (SASP) that can drive or exacerbate several age-related pathologies, including cancer. Flavonoids, including apigenin, were recently shown to reduce the SASP of a human fibroblast strain induced to senesce by bleomycin. Here, we confirm that apigenin suppresses the SASP in three human fibroblast strains induced to senesce by ionizing radiation, constitutive MAPK (mitogen-activated protein kinase) signaling, oncogenic RAS, or replicative exhaustion. Apigenin suppressed the SASP in part by suppressing IL-1α signaling through IRAK1 and IRAK4, p38-MAPK, and NF-κB. Apigenin was particularly potent at suppressing the expression and secretion of CXCL10 (IP10), a newly identified SASP factor. Further, apigenin-mediated suppression of the SASP substantially reduced the aggressive phenotype of human breast cancer cells, as determined by cell proliferation, extracellular matrix invasion, and epithelial-mesenchymal transition. Our results support the idea that apigenin is a promising natural product for reducing the impact of senescent cells on age-related diseases such as cancer.
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      dateModified:2017-04-04T00:00:00Z
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         Human fibroblasts
         Proliferation
         Invasion
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         IL-1A
         IRAK1/4
         NF-κB
         Cell Biology
         Geriatrics/Gerontology
         Molecular Medicine
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               type:PostalAddress
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External Links {🔗}(170)

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