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TOPK Inhibition Promotes Anti-Tumor Immunity Via eIF4F Complex Mediated STAT1 Translation in Gastric Cancer.

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Advanced Science (Weinheim, Baden-Wurttemberg, Germany)
|December 19, 2025
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T-lymphokine-activated killer cell-originated protein kinase (TOPK) is a key target in gastric cancer, inhibiting proliferation and immune evasion. Targeting TOPK reshapes the tumor microenvironment, enhancing anti-tumor immunity for improved immunotherapy efficacy.

Keywords:
PD‐L1TOPKgastric cancerimmunometabolic microenvironmentimmunotherapy

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Area of Science:

  • Oncology
  • Immunology
  • Molecular Biology

Background:

  • Immune checkpoint blockade is revolutionary for gastric cancer (GC) but has limited efficacy.
  • Identifying targets that inhibit proliferation and immune evasion is crucial for improving GC treatment.

Purpose of the Study:

  • To identify dual-function targets inhibiting proliferation and immune evasion in gastric cancer.
  • To elucidate the mechanism of T-lymphokine-activated killer cell-originated protein kinase (TOPK) in GC malignancy and immune evasion.

Main Methods:

  • Whole genome-wide CRISPR-Cas9 screening to identify key regulators.
  • In vitro and in vivo mechanistic studies.
  • Analysis of TOPK expression in tumor tissues and correlation with clinical data.

Main Results:

  • TOPK was identified as a key regulator of PD-L1 in GC upon IFN-γ stimulation.
  • TOPK promotes GC malignancy and immune evasion by enhancing STAT1 translation via the eIF4F complex.
  • This leads to PD-L1 and IDO1 overexpression, causing immunometabolic suppression.
  • Higher TOPK levels correlate with advanced clinical stages, reduced efficacy, and poorer survival.

Conclusions:

  • The IFN-γ-TOPK-eIF4F-STAT1-PD-L1/IDO1 axis is a critical regulator of the tumor immunometabolic microenvironment in GC.
  • TOPK inhibitors can reshape the tumor immunometabolic microenvironment to enhance anti-tumor immunity.
  • Targeting TOPK offers novel insights for combining targeted therapy with immunotherapy in GC treatment.