AI Article Synopsis
- The study investigates how ethanol and its metabolites might affect breast tumor cell growth, particularly through signaling pathways important for cell proliferation.
- Ethanol treatment on MCF-7 breast cancer cells led to a significant increase in p44/42 MAPK activity (about 400%), suggesting that these signaling pathways are influenced by ethanol.
- Additionally, the findings demonstrated that the increased p44/42 MAPK activity corresponded to a 200% rise in cell growth, indicating that the Ras/MEK/MAPK pathway plays a key role in how ethanol promotes the growth of breast cancer cells.
Article Abstract
The role of ethanol or its metabolites on breast neoplasm has not been characterized. We hypothesized that ethanol may alter the growth rate of human breast tumor epithelial cells by modulating putative growth-promoting signaling pathways such as p44/42 mitogen-activated protein kinases (MAPKs). The MCF-7 cell line, considered a suitable model, was used in these studies to investigate the effects of ethanol on [(3)H]thymidine incorporation, cell number, and p44/42 MAPK activities in the presence or absence of a MAPK or extracellular signal-regulated kinase ERK-1, and (MEK1) inhibitor (PD098059). Treatment of MCF-7 cells with a physiologically relevant concentration of ethanol (0.3% or 65 mM) increased p44/42 activities by an average of 400% (P < 0.02), and subsequent cell growth by 200% (P < 0.05) in a MEK1 inhibitor (PD098059)-sensitive fashion, thus suggesting that the Ras/MEK/MAPK signaling pathways are crucial for ethanol-induced MCF-7 cell growth.
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| http://dx.doi.org/10.1177/153537020222700406 | DOI Listing |
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