NFATc2 promotes lactate and M2 macrophage polarization through USP17 in lung adenocarcinoma

Author:

Wang Liang1,Huang Miao1,Zhang Shanyuan1,Yang Yue1,Huang Bo2

Affiliation:

1. Peking University Cancer Hospital and Institute

2. The First Affiliated Hospital of Liaoning Medical University

Abstract

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

Publisher

Research Square Platform LLC

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