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Updated: Aug 21, 2026

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Published on: July 21, 2018

AURKB-mediated phosphorylation of metabolic enzyme CD73 drives immune suppression and renal cell carcinoma

Tianyu Tang1,2, Wuping Yang3, Minghao Lu3

  • 1Department of Urology, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China. tangtianyu0701@zju.edu.cn.

Cell Death and Differentiation
|August 19, 2026
PubMed

Insights

Aurora kinase B (AURKB) drives CD73 overexpression in renal cell carcinoma (RCC), promoting immune suppression and immunotherapy resistance. Targeting AURKB stabilizes CD73, restoring antitumor immunity and enhancing checkpoint blockade efficacy.

Area of Science:

  • Oncology
  • Immunology
  • Molecular Biology

Background:

  • Aberrant tumor metabolism fuels an immunosuppressive tumor microenvironment.
  • CD73 overexpression elevates extracellular adenosine, suppressing antitumor immunity and causing immunotherapy resistance.
  • Mechanisms of CD73 upregulation in tumors are not well understood.

Purpose of the Study:

  • Identify regulators of CD73 overexpression in renal cell carcinoma (RCC).
  • Elucidate the role of AURKB in CD73-mediated immune evasion and immunotherapy resistance.
  • Investigate AURKB as a therapeutic target to enhance immunotherapy efficacy in RCC.

Main Methods:

  • Analysis of AURKB expression in RCC tissues.
  • Investigating the mechanistic link between AURKB and CD73 expression.
  • Mass cytometry (CyTOF) to assess immune cell infiltration and exhaustion.
  • In vivo studies evaluating AURKB inhibition in combination with immune checkpoint blockade.

Main Results:

  • AURKB is highly expressed in RCC and correlates with poor prognosis in immunogenic tumors.
  • AURKB enhances CD73 expression and promotes T cell dysfunction and immune suppression.
  • AURKB directly phosphorylates CD73, inhibiting its degradation and stabilizing its expression.
  • AURKB inhibition restores antitumor immunity and synergizes with immune checkpoint blockade in vivo.

Conclusions:

  • AURKB is a critical regulator of CD73 overexpression in RCC, driving immune evasion.
  • The AURKB-CD73 axis represents a novel mechanism of immunotherapy resistance.
  • Targeting AURKB offers a promising strategy to enhance immunotherapy efficacy in RCC.

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