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  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
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We are analyzing https://link.springer.com/article/10.1007/s13277-012-0543-8.

Title:
Effect of TRAF6 on the biological behavior of human lung adenocarcinoma cell | Tumor Biology
Description:
Tumor necrosis factor receptor-associated factor 6 (TRAF6) is a unique adaptor protein of the tumor necrosis factor receptor-associated factor family that mediates both tumor necrosis factor receptor and interleukin-1 receptor/Toll-like receptor signaling. A recent study showed that TRAF6 played an important role in tumorigenesis and invasion through activation of nuclear factor kappa B (NF-ĪŗB). However, the biological role of TRAF6 remains unknown in lung cancer up to now. To address the expression of TRAF6 in lung cancer cells, four lung cancer cell lines (A549, HCC827, NCI-H292, and 95-D) and human bronchial epithelial cells were used to detect the expression of TRAF6 protein by western blotting. Results indicated that TRAF6 displayed an upregulation in human lung cancer cell lines. To investigate the effects of TRAF6 on the biological behavior of human lung adenocarcinoma cell, we generated human lung adenocarcinoma A549 cell line in which TRAF6 was depleted. The results showed that downregulation of TRAF6 could decrease cell viability, suppress cell proliferation and invasion, and promote cell apoptosis. At the same time, we explored the effects of TRAF6 on the expression of the following proteins: phosphor-NF-ĪŗB (p-p65), cyclin D1, caspase-3, and matrix metalloproteinase 9 (MMP9). Downregulation of TRAF6 could decrease the expression of p-p65, cyclin D1, and MMP9 and increase the expression of caspase-3. All these results suggested that TRAF6 might be involved in the potentiation of growth, proliferation, and invasion of A549 cell line, as well as the inhibition of A549 cell apoptosis by the activation of NF-ĪŗB. To make a long story short, the overexpression of TRAF6 might be related to the tumorigenesis and invasion of lung cancer.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {šŸ“š}

  • Education
  • Telecommunications
  • Health & Fitness

Content Management System {šŸ“}

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 {šŸ“ˆ}

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? {šŸ’ø}

We're unsure if the website is profiting.

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 might be making money, but it's not detectable how they're doing it.

Keywords {šŸ”}

article, google, scholar, pubmed, cas, traf, cell, cancer, factor, lung, activation, tumor, signaling, invasion, biol, necrosis, nfkappab, protein, nuclear, human, receptor, cells, wang, chem, proliferation, receptorassociated, expression, apoptosis, kinase, res, mol, factorkappab, chen, family, access, zhang, privacy, cookies, content, growth, carcinoma, pathway, inhibits, gene, products, sun, publish, research, search, biological,

Topics {āœ’ļø}

uv-induced nf-kappab activation transcription factor nf-kappab nf-kappab-inducing kinase nf-kappab/cyclin d1 pathway month download article/chapter glycogen synthase kinase-3beta suppressing nuclear factor-kappab traf-6/tak-1 protein complex lung cancer biomarkers cytokine-induced mmp-9 synthesis nuclear factor-kappab signaling nuclear factor-kappab activation early-stage lung adenocarcinomas ret/ptc fusion oncoprotein tumor necrosis factor promote cell apoptosis nf-kappab pathways paracrine tnfalpha signalling nf-kappab activation squamous cell carcinoma nuclear factor-kappab nuclear factor kappab ring-dependent traf6 polyubiquitination nf-kappab activator ikappabalpha kinase activation transforming activities emanating a549 cell line growth factor receptor-1 human lung cancer full article pdf factor family protein ubiquitin-specific protease 4 alpha kinase interleukin-1 receptor/toll traf2-mediated activation nuclear factor kappa unique adaptor protein lung cancer risk putative signal transducers lung cancer cells privacy choices/manage cookies apoptotic genes induced human colorectal cancer a549 cell apoptosis cancer cell survival human breast cancer factor protein inhibits cellular invasion /interleukin-1 receptor signaling phosphor-nf-Īŗb

Questions {ā“}

  • Lung cancer and lung stem cells: strange bedfellows?

Schema {šŸ—ŗļø}

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         headline:Effect of TRAF6 on the biological behavior of human lung adenocarcinoma cell
         description:Tumor necrosis factor receptor-associated factor 6 (TRAF6) is a unique adaptor protein of the tumor necrosis factor receptor-associated factor family that mediates both tumor necrosis factor receptor and interleukin-1 receptor/Toll-like receptor signaling. A recent study showed that TRAF6 played an important role in tumorigenesis and invasion through activation of nuclear factor kappa B (NF-ĪŗB). However, the biological role of TRAF6 remains unknown in lung cancer up to now. To address the expression of TRAF6 in lung cancer cells, four lung cancer cell lines (A549, HCC827, NCI-H292, and 95-D) and human bronchial epithelial cells were used to detect the expression of TRAF6 protein by western blotting. Results indicated that TRAF6 displayed an upregulation in human lung cancer cell lines. To investigate the effects of TRAF6 on the biological behavior of human lung adenocarcinoma cell, we generated human lung adenocarcinoma A549 cell line in which TRAF6 was depleted. The results showed that downregulation of TRAF6 could decrease cell viability, suppress cell proliferation and invasion, and promote cell apoptosis. At the same time, we explored the effects of TRAF6 on the expression of the following proteins: phosphor-NF-ĪŗB (p-p65), cyclin D1, caspase-3, and matrix metalloproteinase 9 (MMP9). Downregulation of TRAF6 could decrease the expression of p-p65, cyclin D1, and MMP9 and increase the expression of caspase-3. All these results suggested that TRAF6 might be involved in the potentiation of growth, proliferation, and invasion of A549 cell line, as well as the inhibition of A549 cell apoptosis by the activation of NF-ĪŗB. To make a long story short, the overexpression of TRAF6 might be related to the tumorigenesis and invasion of lung cancer.
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      headline:Effect of TRAF6 on the biological behavior of human lung adenocarcinoma cell
      description:Tumor necrosis factor receptor-associated factor 6 (TRAF6) is a unique adaptor protein of the tumor necrosis factor receptor-associated factor family that mediates both tumor necrosis factor receptor and interleukin-1 receptor/Toll-like receptor signaling. A recent study showed that TRAF6 played an important role in tumorigenesis and invasion through activation of nuclear factor kappa B (NF-ĪŗB). However, the biological role of TRAF6 remains unknown in lung cancer up to now. To address the expression of TRAF6 in lung cancer cells, four lung cancer cell lines (A549, HCC827, NCI-H292, and 95-D) and human bronchial epithelial cells were used to detect the expression of TRAF6 protein by western blotting. Results indicated that TRAF6 displayed an upregulation in human lung cancer cell lines. To investigate the effects of TRAF6 on the biological behavior of human lung adenocarcinoma cell, we generated human lung adenocarcinoma A549 cell line in which TRAF6 was depleted. The results showed that downregulation of TRAF6 could decrease cell viability, suppress cell proliferation and invasion, and promote cell apoptosis. At the same time, we explored the effects of TRAF6 on the expression of the following proteins: phosphor-NF-ĪŗB (p-p65), cyclin D1, caspase-3, and matrix metalloproteinase 9 (MMP9). Downregulation of TRAF6 could decrease the expression of p-p65, cyclin D1, and MMP9 and increase the expression of caspase-3. All these results suggested that TRAF6 might be involved in the potentiation of growth, proliferation, and invasion of A549 cell line, as well as the inhibition of A549 cell apoptosis by the activation of NF-ĪŗB. To make a long story short, the overexpression of TRAF6 might be related to the tumorigenesis and invasion of lung cancer.
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External Links {šŸ”—}(175)

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