ArticleJournal of cancer prevention2014
Ethanol Mediates Cell Cycle Arrest and Apoptosis in SK-N-SH Neuroblastoma Cells.
Article in Journal of cancer prevention, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
2 citing papers in PubMed, 2 citations in OpenAlex.
- Binge ethanol exposure increases the Krüppel-like factor 11-monoamine oxidase (MAO) pathway in rats: Examining the use of MAO inhibitors to prevent ethanol-induced brain injury.Neuropharmacology · 2016Article
- On Gelsemium and Complementary and Alternative Medicine (CAM) in Anxiety and Experimental Neurology.Neurology and therapy · 2015Article
Corrections and comments
- Retraction · 2015-06-01Duplication of Text ·
- Retracted
Authors and funding
3 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe mechanisms of cell or organ damage by chronic alcohol consumption are still poorly understood. The present study aimed to investigate the role of the mitogen-activated protein kinases during ethanol-induced damage to SK-N-SH neuroblastoma cells.
methodsCells were treated with ethanol and subsequently analyzed for cell morphology, viability, and DNA fragmentation. Immunoblot analysis was performed to assess various proteins levels associated with cell cycle arrest and apoptosis after ethanol exposure.
resultsEthanol induced time- and dose-dependent cell death in SK-N-SH cells and increased c-Jun N-terminal protein kinase (JNK) activity in a time- and concentration dependent manner. In contrast, p38 kinase activity increased transiently. After treatment with JNK or p38 kinase inhibitors, ethanol-induced cell death significantly reduced. Ethanol-induced cell death was accompanied by increased cytochrome c release and caspase 3 activity observed at 12 h. In contrast, the level of anti-apoptotic Bcl-2 protein did not change. Ethanol also increased the phosphorylation of p53 and p53 activation was followed by an increase in the p21 tumor suppressor protein accompanied by a gradual decrease in phospho-Rb protein.
conclusionOur results suggest that ethanol mediates apoptosis of neuroblastoma cells by stimulating p53-related cell cycle arrest mediated through activation of the JNK-related pathway.
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Registered trials
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