Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA.
Computational and Systems Biology Program, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA.
Science. 2020 Jul 17;369(6501):276-282. doi: 10.1126/science.aaz2193.
The tumor microenvironment plays a critical regulatory role in cancer progression, especially in central nervous system metastases. Cancer cells within the cerebrospinal fluid (CSF)-filled leptomeninges face substantial microenvironmental challenges, including inflammation and sparse micronutrients. To investigate the mechanism by which cancer cells in these leptomeningeal metastases (LM) overcome these constraints, we subjected CSF from five patients with LM to single-cell RNA sequencing. We found that cancer cells, but not macrophages, within the CSF express the iron-binding protein lipocalin-2 (LCN2) and its receptor SCL22A17. These macrophages generate inflammatory cytokines that induce cancer cell LCN2 expression but do not generate LCN2 themselves. In mouse models of LM, cancer cell growth is supported by the LCN2/SLC22A17 system and is inhibited by iron chelation therapy. Thus, cancer cells appear to survive in the CSF by outcompeting macrophages for iron.
肿瘤微环境在癌症进展中起着关键的调节作用,特别是在中枢神经系统转移中。在充满脑脊液(CSF)的软脑膜中,癌细胞面临着巨大的微环境挑战,包括炎症和稀疏的微量营养素。为了研究脑脊液中脑膜转移(LM)癌细胞如何克服这些限制,我们对来自五名 LM 患者的 CSF 进行了单细胞 RNA 测序。我们发现 CSF 中的癌细胞,但不是巨噬细胞,表达铁结合蛋白 lipocalin-2(LCN2)及其受体 SCL22A17。这些巨噬细胞产生诱导癌细胞 LCN2 表达的炎症细胞因子,但自身不产生 LCN2。在 LM 的小鼠模型中,癌细胞的生长受到 LCN2/SLC22A17 系统的支持,并受到铁螯合疗法的抑制。因此,癌细胞似乎通过与巨噬细胞竞争铁来在 CSF 中存活。