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CIP2A Constrains Th17 Differentiation by Modulating STAT3 Signaling

Mohd Moin Khan1, Ubaid Ullah2, Meraj H Khan2

  • 1Turku Bioscience Centre, University of Turku and Åbo Akademi University, Tykistökatu 6A, Turku, Finland; Turku Doctoral Programme of Molecular Medicine (TuDMM), University of Turku, Turku, Finland.

Iscience
|March 15, 2020
PubMed

Insights

Cancerous Inhibitor of Protein Phosphatase 2A (CIP2A) negatively regulates IL-17 production in immune cells. This study reveals CIP2A

Area of Science:

  • Immunology
  • Molecular Biology
  • Cancer Research

Background:

  • Cancerous Inhibitor of Protein Phosphatase 2A (CIP2A) is an oncogene and a potential cancer therapy target.
  • Understanding CIP2A's function in immune cells is crucial for cancer therapy development.

Purpose of the Study:

  • To investigate the role of CIP2A in regulating interleukin-17 (IL-17) production by T helper 17 (Th17) cells.
  • To elucidate the molecular mechanisms by which CIP2A influences Th17 cell function.

Main Methods:

  • Analysis of IL-17 production in CIP2A-deficient and sufficient human and mouse Th17 cells.
  • Assessment of STAT3 phosphorylation dynamics.
  • Interactome analysis of phosphorylated STAT3.
  • Genome-wide gene expression profiling.

Main Results:

  • CIP2A deficiency leads to increased IL-17 production and enhanced/prolonged STAT3 phosphorylation in Th17 cells.
  • CIP2A regulates Acylglycerol Kinase (AGK) interaction with STAT3.
  • This interaction modulates STAT3 phosphorylation and IL-17 expression.

Conclusions:

  • CIP2A acts as a negative regulator of IL-17 production in Th17 cells.
  • CIP2A influences Th17 differentiation and function through its regulation of the AGK-STAT3 interaction.
  • Targeting CIP2A may offer a therapeutic strategy for immune-mediated diseases and cancers.
Keywords:
ImmunologyMolecular InteractionOmicsSystems Biology

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