期刊
ISCIENCE
卷 23, 期 3, 页码 -出版社
CELL PRESS
DOI: 10.1016/j.isci.2020.100947
关键词
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资金
- BioCenter Finland
- University of Turku graduate school on Turku Doctoral Programme of Molecular Medicine (TuDMM)
- Finnish Cultural Foundation
- Academy of Finland, AoF, Centre of Excellence in Molecular Systems Immunology and Physiology Research (2012-2017) [250114]
- AoF [292335, 294337, 292482, 31444]
- JDRF
- Finnish Cancer Foundation
- Sigrid Juselius Foundation
- Academy of Finland [258313]
- Academy of Finland (AKA) [258313, 258313] Funding Source: Academy of Finland (AKA)
Cancerous Inhibitor of Protein Phosphatase 2A (CIP2A) is an oncogene and a potential cancer therapy target protein. Accordingly, a better understanding of the physiological function of CIP2A, especially in the context of immune cells, is a prerequisite for its exploitation in cancer therapy. Here, we report that CIP2A negatively regulates interleukin (IL)-17 production by Th17 cells in human and mouse. Interestingly, concomitant with increased IL-17 production, CIP2A-deficient Th17 cells had increased strength and duration of STAT3 phosphorylation. We analyzed the interactome of phosphorylated STAT3 in CIP2A-deficient and CIP2A-sufficient Th17 cells and indicated together with genome-wide gene expression profiling, a role of Acylglycerol Kinase (AGK) in the regulation of Th17 differentiation by CIP2A. We demonstrated that CIP2A regulates the strength of the interaction between AGK and STAT3, and thereby modulates STAT3 phosphorylation and expression of IL-17 in Th17 cells.
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