Although epidemiological evidence has confirmed the role of heavy alcohol consumption as an established risk factor for esophageal, liver, and breast cancers, the molecular mechanisms underlying this effect are not fully understood, particularly with regard to breast cancer. In this study, expression of the
retinoic acid early inducible-1 (RAE-1) gene was determined in mice adipocytes. RAE-1 is a ligand of the natural-killer group 2 member D (NKG2D) receptor, which plays a crucial role in tumor immunity. RT-PCR and Western blotting analysis demonstrated that TNF-α treatment induced
RAE-1 mRNA and RAE-1 protein expression in adipocytes obtained from differentiated 3T3-F442A cells. Real-time RT-PCR analysis showed that 300 mM ethanol enhanced
RAE-1 mRNA expression, which peaked 6 h after administration. In addition,
RAE-1 mRNA was detected in visceral adipose tissue obtained from mice. These observations indicate that
RAE-1 mRNA is expressed in adipocytes and that its expression is enhanced by TNF-α, which has been shown to be induced in adipose tissue by long-term alcohol consumption. Furthermore, ethanol directly enhanced
RAE-1 mRNA expression, suggesting that alcohol consumption enhances RAE-1 expression in adipose tissue and might modify tumor immunity. This finding might provide novel insight into the mechanism of alcohol-associated carcinogenesis.
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