Center for Epigenetics & Disease Prevention, Texas A&M Health, Houston, TX 77030, USA.
Department of Translational Medical Sciences, Texas A&M College of Medicine, Houston, TX 77030, USA.
Nutrients. 2024 Jan 30;16(3):396. doi: 10.3390/nu16030396.
Cancer etiology involves complex interactions between genetic and non-genetic factors, with epigenetic mechanisms serving as key regulators at multiple stages of pathogenesis. Poor dietary habits contribute to cancer predisposition by impacting DNA methylation patterns, non-coding RNA expression, and histone epigenetic landscapes. Histone post-translational modifications (PTMs), including acyl marks, act as a molecular code and play a crucial role in translating changes in cellular metabolism into enduring patterns of gene expression. As cancer cells undergo metabolic reprogramming to support rapid growth and proliferation, nuanced roles have emerged for dietary- and metabolism-derived histone acylation changes in cancer progression. Specific types and mechanisms of histone acylation, beyond the standard acetylation marks, shed light on how dietary metabolites reshape the gut microbiome, influencing the dynamics of histone acyl repertoires. Given the reversible nature of histone PTMs, the corresponding acyl readers, writers, and erasers are discussed in this review in the context of cancer prevention and treatment. The evolving 'acyl code' provides for improved biomarker assessment and clinical validation in cancer diagnosis and prognosis.
癌症的病因涉及遗传和非遗传因素之间的复杂相互作用，表观遗传机制在发病机制的多个阶段充当关键调节剂。不良的饮食习惯通过影响 DNA 甲基化模式、非编码 RNA 表达和组蛋白表观遗传景观，导致癌症易感性。组蛋白翻译后修饰（PTMs），包括酰基标记，充当分子密码，在将细胞代谢变化转化为持久的基因表达模式方面发挥着关键作用。随着癌细胞经历代谢重编程以支持快速生长和增殖，饮食和代谢衍生的组蛋白酰基变化在癌症进展中的细微作用已经显现出来。除了标准的乙酰化标记之外，特定类型和机制的组蛋白酰化揭示了饮食代谢物如何重塑肠道微生物组，影响组蛋白酰基谱的动态。鉴于组蛋白 PTM 的可逆性质，在本综述中，根据癌症的预防和治疗，讨论了相应的酰基读取器、写入器和橡皮擦。不断发展的“酰基密码”为癌症诊断和预后中的生物标志物评估和临床验证提供了改进。
