The epigenome coordinates spatial-temporal specific gene expression during development and in adulthood, for the maintenance of homeostasis and upon tissue repair. The upheaval of the epigenetic landscape is a key event in the onset of many pathologies including tumours, where epigenetic changes cooperate with genetic aberrations to establish the neoplastic phenotype and to drive cell plasticity during its evolution. DNA methylation, histone modifiers and readers or other chromatin components are indeed often altered in cancers, such as carcinomas that develop in epithelia. Lining the surfaces and the cavities of our body and acting as a barrier from the environment, epithelia are frequently subjected to acute or chronic tissue damages, such as mechanical injuries or inflammatory episodes. These events can activate plasticity mechanisms, with a deep impact on cells’ epigenome. Despite being very effective, tissue repair mechanisms are closely associated with tumour onset. Here we review the similarities between tissue repair and carcinogenesis, with a special focus on the epigenetic mechanisms activated by cells during repair and opted by carcinoma cells in multiple epithelia. Moreover, we discuss the recent findings on inflammatory and wound memory in epithelia and describe the epigenetic modifications that characterise them. Finally, as wound memory in epithelial cells promotes carcinogenesis, we highlight how it represents an early step for the establishment of field cancerization.

表观基因组在发育和成年期间协调时空特定基因表达，以维持体内平衡和组织修复。表观遗传景观的剧变是包括肿瘤在内的许多病理学发病的关键事件，其中表观遗传变化与遗传畸变共同建立肿瘤表型并在其进化过程中驱动细胞可塑性。 DNA 甲基化、组蛋白修饰剂和读取器或其他染色质成分确实经常在癌症中发生改变，例如在上皮细胞中发生的癌。上皮细胞排列在我们身体的表面和体腔内，充当环境的屏障，经常遭受急性或慢性组织损伤，例如机械损伤或炎症发作。这些事件可以激活可塑性机制，对细胞的表观基因组产生深远的影响。尽管组织修复机制非常有效，但它与肿瘤的发生密切相关。在这里，我们回顾了组织修复和癌发生之间的相似性，特别关注修复过程中细胞激活的表观遗传机制以及多个上皮细胞中癌细胞选择的表观遗传机制。此外，我们讨论了关于上皮细胞炎症和伤口记忆的最新发现，并描述了表征它们的表观遗传修饰。最后，由于上皮细胞中的伤口记忆促进癌变，我们强调它如何代表了区域癌化建立的早期步骤。