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November 19, 2025Protein & CellOpen Access

Tumor cell-specific loss of GPX4 reprograms triacylglycerol metabolism to escape ferroptosis and impair antitumor immunity in NSCLC

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Authors

PWPeng WangSZShengdan ZhangXCXin Chen

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Overview

Inducible knockout of GPX4 promotes tumor progression in NSCLC, suggesting therapeutic strategies targeting lipid metabolism.

Key Points

  • This research aims to elucidate the role of GPX4 in tumor progression and immune evasion in non-small cell lung cancer.
  • Utilized inducible knockout of GPX4 in tumor cells of mouse models of NSCLC.
  • Analyzed the effects on tumor progression using Kras LSL-G12D/+ Lkb1 fl/fl and Kras LSL-G12D/+ Tp53 fl/fl models.
  • Investigated lipid metabolism by measuring triacylglycerol synthesis and secretion, and CD8+ T cell activation.
  • GPX4 deletion enhances NSCLC progression by promoting triacylglycerol synthesis in tumor cells.
  • Upregulation of DGAT1/2 in GPX4-deficient cells facilitates lipid droplet formation and secretion of lipid molecules.
  • Inhibition of DGAT1/2 or restoration of GPX4 resensitizes tumor cells to ferroptosis and activates antitumor T cells.

Cite This Study

Wang et al. (2025) studied this question.

synapsesocial.com/papers/6924f091c0ce034ddc350a89https://doi.org/10.1093/procel/pwaf101
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1GPX4 in the Tumor Microenvironment: Not Just Inhibiting Ferroptosis, but Immuno-Metabolic Regulation2026
  2. 2GPX4 is a key ferroptosis regulator orchestrating T cells and CAR-T-cells sensitivity to ferroptosis2025 · 22 citations
  3. 3Beyond catalysis: Spatial topology of GPX4 in ferroptosis and its theranostic implications2026
  4. 4GPX4 Inhibitor Resistance and Metastatic Features in Triple‐Negative Breast Cancer2026
  5. 5METTL16-dependent GPX4 m6A modification links ferroptosis to NSCLC TKIs resistance2025 · 5 citations