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Stanniocalcin 1 is a phagocytosis checkpoint driving tumor immune resistance

Heng Lin1, Ilona Kryczek1, Shasha Li2

  • 1Department of Surgery, University of Michigan School of Medicine, Ann Arbor, MI, USA; Center of Excellence for Cancer Immunology and Immunotherapy, University of Michigan Rogel Cancer Center, University of Michigan School of Medicine, Ann Arbor, MI, USA.

Cancer Cell
|January 29, 2021
PubMed

Insights

Tumor stanniocalcin 1 (STC1) hinders cancer immunotherapy by blocking phagocytosis. Targeting STC1 may improve treatment responses by restoring immune cell function and overcoming therapeutic resistance.

Area of Science:

  • Oncology
  • Immunology
  • Molecular Biology

Background:

  • Immunotherapy offers durable responses in some cancer patients but faces challenges with therapeutic resistance.
  • Tumor stanniocalcin 1 (STC1) expression is linked to immunotherapy efficacy and patient survival across various cancers.

Purpose of the Study:

  • To investigate the role of tumor STC1 in tumor progression and resistance to cancer immunotherapy.
  • To elucidate the mechanism by which STC1 influences anti-tumor immunity and phagocytosis.

Main Methods:

  • Utilized gain- and loss-of-function experiments in murine tumor models.
  • Investigated the interaction between STC1 and calreticulin (CRT) in tumor immune evasion.
  • Assessed the impact of STC1 on antigen-presenting cell (APC) function and T cell activation.

Main Results:

  • Tumor STC1 expression correlates with reduced immunotherapy efficacy and poorer patient survival.
  • STC1 promotes tumor progression and resistance to checkpoint blockade therapy.
  • STC1 inhibits phagocytosis by APCs by minimizing membrane exposure of the 'eat-me' signal CRT.
  • This abrogates APC-mediated antigen presentation and T cell activation, leading to tumor immune evasion.

Conclusions:

  • Tumor STC1 acts as a novel phagocytosis checkpoint, contributing to immune evasion and immunotherapy resistance.
  • Targeting STC1 and its interaction with CRT presents a potential strategy to enhance cancer immunotherapy efficacy.
Keywords:
PD-1T cell immunitycalreticulincheckpointdendritic celleat-me signalmacrophagesphagocytosisstanniocalcin 1tumor

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