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Co-immunoprecipitation Assay for Studying Functional Interactions Between Receptors and Enzymes
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Protein Kinase D3 Promotes the Reconstruction of OSCC Immune Escape Niche Via Regulating MHC-I and Immune Inhibit

Die Lv1, Jiao Chen, Yingzhu Kang

  • 1State Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, Sichuan Province, People's Republic of China.

Journal of Immunotherapy (Hagerstown, Md. : 1997)
|September 21, 2021
PubMed

Insights

Protein kinase D3 (PKD3) promotes oral cancer immune escape by altering immune-related molecules like PD-L1 and MHC-I. This impacts the tumor microenvironment and T cell responses, highlighting PKD3 as a potential therapeutic target.

Area of Science:

  • Oncology
  • Immunology
  • Molecular Biology

Background:

  • Protein kinase D3 (PKD3) is implicated in various cancers.
  • Its role in tumor immune escape, particularly in oral squamous cell carcinoma (OSCC), is largely unexplored.

Purpose of the Study:

  • To investigate the function and mechanism of PKD3 in shaping the immune escape niche of OSCC.
  • To determine PKD3's impact on key immune regulatory molecules within the tumor microenvironment.

Main Methods:

  • Western blotting analysis of OSCC cells.
  • Gene expression correlation analysis using The Cancer Genome Atlas (TCGA) data.
  • PKD3 knockdown and overexpression experiments in OSCC and precancerous cells.
  • Measurement of cytokine secretion.
  • T lymphocyte activation assays.

Main Results:

  • PKD3 expression positively correlated with Fas and PD-L1, and negatively with MHC-I in OSCC.
  • PKD3 knockdown decreased Fas and PD-L1, increased MHC-I, and reduced secretion of TGF-β, CCL21, and IL-10.
  • PKD3 overexpression showed opposite effects.
  • Tumor antigens from PKD3-knockdown cells enhanced T lymphocyte growth and activation.

Conclusions:

  • PKD3 promotes OSCC immune escape by modulating Fas, PD-L1, MHC-I, TGF-β, CCL21, and IL-10.
  • PKD3 plays a critical role in reconstructing the tumor immune escape niche.
  • Targeting PKD3 may offer a strategy to overcome immune evasion in OSCC.

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