黑色素瘤由转化的黑色素细胞产生，位于表皮基底层的真皮-表皮交界处。黑色素细胞完全被角质形成细胞邻居包围，它们通过直接接触和旁分泌信号传导与角质形成细胞进行交流，以维持正常的生长控制和体内平衡。来自阳光的紫外线辐射重塑了这个通讯网络，以驱动保护性晒黑反应。然而，反复的阳光照射会导致黑色素细胞突变的积累，这些突变被认为是黑色素瘤发生和进展的主要驱动因素。现在很清楚，黑素细胞的突变不足以驱动肿瘤的形成——肿瘤环境起着关键作用。本综述重点关注促进黑色素瘤发生和进展的黑色素细胞-角质形成细胞通讯的变化，特别关注最近的机制见解，这些见解为开发拦截黑色素瘤发展的新方法奠定了基础。© 2024 作者。 BioEssays 由 Wiley periodicals LLC 出版。

Melanomas arise from transformed melanocytes, positioned at the dermal-epidermal junction in the basal layer of the epidermis. Melanocytes are completely surrounded by keratinocyte neighbors, with which they communicate through direct contact and paracrine signaling to maintain normal growth control and homeostasis. UV radiation from sunlight reshapes this communication network to drive a protective tanning response. However, repeated rounds of sun exposure result in accumulation of mutations in melanocytes that have been considered as primary drivers of melanoma initiation and progression. It is now clear that mutations in melanocytes are not sufficient to drive tumor formation-the tumor environment plays a critical role. This review focuses on changes in melanocyte-keratinocyte communication that contribute to melanoma initiation and progression, with a particular focus on recent mechanistic insights that lay a foundation for developing new ways to intercept melanoma development.© 2024 The Author(s). BioEssays published by Wiley Periodicals LLC.