It is well known that immune cells including macrophages within the tumor microenvironment play an essential role in tumor progression. Here, we studied how NFATc2 regulated macrophage properties in lung adenocarcinoma. Higher expression of NFATc2 was observed in the lung adenocarcinoma tissues than in the normal lung tissues. Positive relationships were found between NFATc2 and genes associated with hypoxia and glycolysis in lung adenocarcinoma from the TCGA dataset. According to single-cell sequence data, NFATc2 was closely associated with infiltrating immune cells and was related to macrophage polarization. As a transcription factor, NFATc2 binding to the USP17 promoter region, that enhanced cell migration and lactate level in lung adenocarcinoma cells, and M2 polarization in macrophages. Furthermore, the NFATc2 inhibitor suppressed lactate and M2 macrophage polarization induced by NFATc2 and USP17. In conclusion, NFATc2 promotes lactate level and M2 macrophage polarization by transcriptionally regulating USP17 in lung adenocarcinoma.

中文翻译：

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NFATc2 通过 USP17 在肺腺癌中促进乳酸和 M2 巨噬细胞极化。

众所周知，肿瘤微环境中的免疫细胞（包括巨噬细胞）在肿瘤进展中发挥着重要作用。在这里，我们研究了 NFATc2 如何调节肺腺癌中的巨噬细胞特性。NFATc2在肺腺癌组织中的表达量高于正常肺组织。从 TCGA 数据集中发现，NFATc2 与肺腺癌缺氧和糖酵解相关基因之间存在正相关关系。单细胞序列数据显示，NFATc2与浸润性免疫细胞密切相关，并与巨噬细胞极化相关。作为转录因子，NFATc2 与 USP17 启动子区域结合，增强肺腺癌细胞的细胞迁移和乳酸水平，以及巨噬细胞的 M2 极化。此外，NFATc2 抑制剂抑制了 NFATc2 和 USP17 诱导的乳酸和 M2 巨噬细胞极化。总之，NFATc2 通过转录调节肺腺癌中的 USP17 促进乳酸水平和 M2 巨噬细胞极化。