Epidemiological evidence underscores alcohol consumption as a strong risk factor for multiple cancer types, with liver cancer being most commonly associated with alcohol intake. While mechanisms linking alcohol consumption to malignant tumors development are not fully understood, the likely players in ethanol-induced carcinogenesis are genotoxic stress caused by formation of acetaldehyde, increased oxidative stress and altered nutrient metabolism, including the impairment of methyl transfer reactions. Alterations of sphingolipid metabolism and associated signaling pathways are another potential link between ethanol and cancer development. In particular, ceramides are involved in the regulation of cellular proliferation, differentiation, senescence and apoptosis and are known to function as important regulators of malignant transformation as well as tumor progression. However, to date, the cross-talk between ceramides and alcohol in cancer disease is largely an open question and only limited data are available on this subject. Most studies linking ceramide to cancer considered liver steatosis as the underlying mechanism, which is not surprising taking into consideration that ceramide pathways are an integral part of the overall lipid metabolism. This review summarizes the latest studies pointing to ceramide as important mediator of cancer-promoting effects of chronic alcohol consumption and underscores the necessity of understanding the role of sphingolipids and lipid signaling in response to alcohol in order to prevent and/or successfully manage diseases caused by alcohol.

流行病学证据强调饮酒是多种癌症类型的重要危险因素，肝癌最常与饮酒有关。虽然将饮酒与恶性肿瘤发展联系起来的机制尚不完全清楚，但乙醇诱导的致癌作用可能是由乙醛形成引起的遗传毒性应激、氧化应激增加和营养代谢改变，包括甲基转移反应受损。鞘脂代谢和相关信号通路的改变是乙醇与癌症发展之间的另一个潜在联系。特别是，神经酰胺参与调节细胞增殖、分化、衰老和细胞凋亡，并且被认为是恶性转化和肿瘤进展的重要调节因子。然而，迄今为止，神经酰胺和酒精在癌症疾病中的相互作用在很大程度上是一个悬而未决的问题，关于这个主题的可用数据有限。大多数将神经酰胺与癌症联系起来的研究都认为肝脏脂肪变性是潜在的机制，考虑到神经酰胺途径是整体脂质代谢的一个组成部分，这并不奇怪。这篇综述总结了神经酰胺作为慢性饮酒促癌作用的重要介质的最新研究，并强调了了解鞘脂和脂质信号在酒精反应中的作用以预防和/或成功管理由酒精引起的疾病的必要性。酒精。