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DOI . ORG {}

  1. Analyzed Page
  2. Matching Content Categories
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  4. Monthly Traffic Estimate
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  6. Keywords
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We began analyzing https://link.springer.com/article/10.1007/s13277-014-1998-6, but it redirected us to https://link.springer.com/article/10.1007/s13277-014-1998-6. The analysis below is for the second page.

Title[redir]:
Crebanine, an aporphine alkaloid, sensitizes TNF-α-induced apoptosis and suppressed invasion of human lung adenocarcinoma cells A549 by blocking NF-κB-regulated gene products | Tumor Biology
Description:
Crebanine is an alkaloid known to exhibit anticancer, but its mechanism is not well understood. Besides, the nuclear factor-kappa B (NF-κB) transcription factor has been correlated with inflammation, carcinogenesis, tumor cell survival, invasion, and angiogenesis. In this study, we investigated the effects of crebanine on tumor necrosis factor alpha (TNF-α)-induced NF-κB activation and the expression of NF-κB-regulated gene products. We found that crebanine reduced the cell proliferation of lung, ovarian, and breast cancer cells. Crebanine also potentiated TNF-α-induced apoptosis which correlated with the suppression of the gene products linked to cell survival, B cell lymphoma-extra large, and proliferation, cyclin D1. In addition, crebanine affected TNF-α-induced activation of caspase-8, caspase-3, and poly(ADP-ribose) polymerase cleavage, indicating that the apoptotic effects of TNF-α were enhanced by crebanine. Moreover, crebanine reduced TNF-α-induced A549 cell invasion and migration. Furthermore, crebanine suppressed the TNF-α-mediated expression of proteins that involved cancer cell invasion (matrix metalloproteinase 9 urokinase-type plasminogen activator, urokinase-type plasminogen activator receptor and intercellular adhesion molecule 1) and angiogenesis (COX-2 and VEGF), all of which are known to be regulated by NF-κB. We also demonstrated that TNF-α induced NF-κB DNA-binding activity, which was inhibited by crebanine. Moreover, crebanine suppressed the TNF-α-induced degradation of inhibitor of NF-κB alpha (IκBa), which led to reduced NF-κB translocation to the nucleus. Taken together, our results demonstrated that crebanine reduced TNF-α-induced cancer cell proliferation, invasion, and survival by suppressing NF-κB activity and expression profile of its downstream genes.

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  • Education
  • Science
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Content Management System {📝}

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Custom-built

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🏙️ Massive Traffic: 50M - 100M visitors per month


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We're unsure how the site profits.

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Keywords {🔍}

article, pubmed, google, scholar, cas, cancer, cell, crebanine, cells, invasion, nfkappab, factor, tumor, human, apoptosis, expression, tnfαinduced, nfκb, gene, products, limtrakul, aggarwal, res, lung, yodkeeree, nuclear, necrosis, activation, proliferation, central, biol, rev, nat, research, pompimon, effects, wang, privacy, cookies, content, angiogenesis, matrix, inhibits, signaling, pathway, stephania, kinase, publish, search, alkaloid,

Topics {✒️}

sensitizes tnf-α-induced apoptosis potentiated tnf-α-induced apoptosis inhibits tnf-alpha-induced apoptosis nf-κb-regulated gene products human tnf-alpha/nf-kappa nf-kappab/ap-1-dependent mechanisms tnf-α-induced degradation induced nf-κb activation tumour-necrosis factor superfamily month download article/chapter reduced nf-κb translocation tnf-α-mediated expression zerumbone abolishes nf-kappab nuclear factor-kappab activation urokinase plasminogen activator regulates nf-kappab activity nf-kappab rnai decreases suppressing nf-κb activity transcription factor nf-kappab tumour necrosis factor cell lymphoma-extra large tnf-alpha signaling tumor necrosis factor breast cancer cells nf-κb alpha nuclear factor-kappab nf-kappab pathway thailand research fund full article pdf gene products linked nuclear factor-kappa nuclear factor kappa suppressing nf-κb kappab kinase pathways human cancer cells metastatic gene products nf-kappab inhibitors regulated matrix metalloproteinases lung cancer cells privacy choices/manage cookies tnf-α metastatic gene expression article yodkeeree tumor cell survival cervical cancer cells regulates icam-1 expression medicine research fund cancer therapy resistance related subjects signal transduction pathway

Schema {🗺️}

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         headline:Crebanine, an aporphine alkaloid, sensitizes TNF-α-induced apoptosis and suppressed invasion of human lung adenocarcinoma cells A549 by blocking NF-κB-regulated gene products
         description:Crebanine is an alkaloid known to exhibit anticancer, but its mechanism is not well understood. Besides, the nuclear factor-kappa B (NF-κB) transcription factor has been correlated with inflammation, carcinogenesis, tumor cell survival, invasion, and angiogenesis. In this study, we investigated the effects of crebanine on tumor necrosis factor alpha (TNF-α)-induced NF-κB activation and the expression of NF-κB-regulated gene products. We found that crebanine reduced the cell proliferation of lung, ovarian, and breast cancer cells. Crebanine also potentiated TNF-α-induced apoptosis which correlated with the suppression of the gene products linked to cell survival, B cell lymphoma-extra large, and proliferation, cyclin D1. In addition, crebanine affected TNF-α-induced activation of caspase-8, caspase-3, and poly(ADP-ribose) polymerase cleavage, indicating that the apoptotic effects of TNF-α were enhanced by crebanine. Moreover, crebanine reduced TNF-α-induced A549 cell invasion and migration. Furthermore, crebanine suppressed the TNF-α-mediated expression of proteins that involved cancer cell invasion (matrix metalloproteinase 9 urokinase-type plasminogen activator, urokinase-type plasminogen activator receptor and intercellular adhesion molecule 1) and angiogenesis (COX-2 and VEGF), all of which are known to be regulated by NF-κB. We also demonstrated that TNF-α induced NF-κB DNA-binding activity, which was inhibited by crebanine. Moreover, crebanine suppressed the TNF-α-induced degradation of inhibitor of NF-κB alpha (IκBa), which led to reduced NF-κB translocation to the nucleus. Taken together, our results demonstrated that crebanine reduced TNF-α-induced cancer cell proliferation, invasion, and survival by suppressing NF-κB activity and expression profile of its downstream genes.
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      headline:Crebanine, an aporphine alkaloid, sensitizes TNF-α-induced apoptosis and suppressed invasion of human lung adenocarcinoma cells A549 by blocking NF-κB-regulated gene products
      description:Crebanine is an alkaloid known to exhibit anticancer, but its mechanism is not well understood. Besides, the nuclear factor-kappa B (NF-κB) transcription factor has been correlated with inflammation, carcinogenesis, tumor cell survival, invasion, and angiogenesis. In this study, we investigated the effects of crebanine on tumor necrosis factor alpha (TNF-α)-induced NF-κB activation and the expression of NF-κB-regulated gene products. We found that crebanine reduced the cell proliferation of lung, ovarian, and breast cancer cells. Crebanine also potentiated TNF-α-induced apoptosis which correlated with the suppression of the gene products linked to cell survival, B cell lymphoma-extra large, and proliferation, cyclin D1. In addition, crebanine affected TNF-α-induced activation of caspase-8, caspase-3, and poly(ADP-ribose) polymerase cleavage, indicating that the apoptotic effects of TNF-α were enhanced by crebanine. Moreover, crebanine reduced TNF-α-induced A549 cell invasion and migration. Furthermore, crebanine suppressed the TNF-α-mediated expression of proteins that involved cancer cell invasion (matrix metalloproteinase 9 urokinase-type plasminogen activator, urokinase-type plasminogen activator receptor and intercellular adhesion molecule 1) and angiogenesis (COX-2 and VEGF), all of which are known to be regulated by NF-κB. We also demonstrated that TNF-α induced NF-κB DNA-binding activity, which was inhibited by crebanine. Moreover, crebanine suppressed the TNF-α-induced degradation of inhibitor of NF-κB alpha (IκBa), which led to reduced NF-κB translocation to the nucleus. Taken together, our results demonstrated that crebanine reduced TNF-α-induced cancer cell proliferation, invasion, and survival by suppressing NF-κB activity and expression profile of its downstream genes.
      datePublished:2014-05-28T00:00:00Z
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External Links {🔗}(223)

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