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Intracellular IL-23R is necessary for mitotic spindle formation and viability in AML

Nathan Duong1,2, Dilshad H Khan1, Geethu E Thomas1

  • 1Princess Margaret Cancer Centre, University Health Network, Toronto, ON, Canada.

Leukemia
|April 17, 2026
PubMed

Insights

Interleukin-23 receptor (IL-23R) is found inside Acute Myeloid Leukemia (AML) cells, not just on the surface. This novel location helps regulate the mitotic spindle, impacting AML cell growth and proliferation.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Hematology
  • Cancer Research

Background:

  • Interleukin-23 receptor (IL-23R) is a known cell surface receptor primarily expressed on T cells, regulating T cell activation.
  • The role and localization of IL-23R in hematological malignancies, particularly Acute Myeloid Leukemia (AML), remain largely unexplored.

Purpose of the Study:

  • To investigate the novel intracellular localization and function of IL-23R in Acute Myeloid Leukemia (AML).
  • To determine the impact of IL-23R's intracellular role on AML cell proliferation and stem cell function.

Main Methods:

  • Comparative analysis of IL-23R expression in primary AML samples versus normal hematopoietic cells.
  • BioID proximity labeling mass spectrometry to identify IL-23R interacting proteins within AML cells.
  • Confirmation of endogenous IL-23R interactions with mitotic spindle proteins using cellular and molecular techniques.
  • Genetic depletion of IL-23R to assess its functional impact on AML cell proliferation and progenitor function.

Main Results:

  • IL-23R expression is significantly increased in primary AML samples compared to normal hematopoietic cells.
  • IL-23R is predominantly localized intracellularly within AML cells, interacting with mitotic spindle proteins via its (S/T)x(I/L)P motif.
  • Genetic depletion of IL-23R disrupts mitotic spindle formation, reduces AML cell proliferation, and impairs stem cell/progenitor function.
  • Depletion of IL-23R does not adversely affect normal hematopoietic cells and progenitors.

Conclusions:

  • IL-23R exhibits a novel intracellular function in regulating mitotic spindle formation within AML cells.
  • Targeting intracellular IL-23R represents a potential therapeutic strategy for Acute Myeloid Leukemia, selectively impacting malignant cells.
  • The findings reveal IL-23R as a key regulator of AML cell growth and stemness.

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