Cancer Res. 2022 May 3;82(9):1692-1694. doi: 10.1158/0008-5472.CAN-22-0940.
Melanomas coopt tumor-draining lymph nodes to support metastatic potential and install immunosuppression. The specific mechanisms that mediate lymph node education, however, remain incompletely understood. In this issue, Rovera and colleagues describe the deactivation of contractile lymph node fibroblasts by dedifferentiated melanoma cells, leading to lymph node expansion and enhanced melanoma invasive potential. Fibroblastic reticular cell relaxation depended upon inhibition of constitutive JAK1/STAT3 and YAP/TAZ signaling, which was mediated in part by tumor secretion of the inflammatory cytokine, IL1. These data support an emerging hypothesis that intrinsic melanoma heterogeneity feeds forward to drive microenvironmental adaptations that mediate invasion and progression. See related article by Rovera et al., p. 1774.
黑色素瘤会利用肿瘤引流的淋巴结来支持转移潜力并建立免疫抑制。然而，介导淋巴结“教育”的具体机制仍不完全清楚。在本期杂志中，Rovera 及其同事描述了去分化的黑色素瘤细胞使具有收缩功能的淋巴结成纤维细胞失活，导致淋巴结扩张和增强黑色素瘤侵袭潜能。成纤维细胞网状细胞的松弛依赖于组成性 JAK1/STAT3 和 YAP/TAZ 信号的抑制，这部分是由肿瘤分泌的炎症细胞因子 IL1 介导的。这些数据支持了一个新兴假说，即内在的黑色素瘤异质性会向前反馈，以驱动介导侵袭和进展的微环境适应。参见 Rovera 等人的相关文章，第 1774 页。
