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September 5, 2025Nature CommunicationsOpen Access

Targeting ALDH16A1 mediated thioredoxin lysosomal degradation to enhance ferroptosis susceptibility in SMARCA4-deficient NSCLC

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Authors

GBGuoshu BiJLJiaqi LiangYBYunyi Bian

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Overview

Observational analysis reveals SMARCA4 deficiency increases ferroptosis resistance in NSCLC, highlighting ALDH16A1's role in therapeutic strategies.

Key Points

  • Ferroptosis susceptibility is enhanced in non-small cell lung cancer due to SMARCA4 deficiency.
  • Reinstating ALDH16A1 or inhibiting thioredoxin improves chemosensitivity in SMARCA4-deficient cells.
  • The study presents a novel dual regulatory axis involving SMARCA4, ALDH16A1, and thioredoxin.
  • Therapies targeting this axis could potentially overcome resistance to chemotherapy in NSCLC.

Cite This Study

Bi et al. (2025) studied this question.

synapsesocial.com/papers/68c23a2cb210217d6477fab9https://doi.org/10.1038/s41467-025-63687-6
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Also Consider

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

  1. 1Targeting NRF2 and FSP1 to Overcome Ferroptosis Resistance in TSC2-Deficient and Cancer Cells2025 · 5 citations
  2. 2Targeting NRF2 and FSP1 to Overcome Ferroptosis Resistance in TSC2-Deficient and Cancer Cells2025
  3. 3Ferroptosis escape in AML stem cells uncovered by single-cell profiling and reversed by STAT3/NRF2 inhibition2025
  4. 4METTL16-dependent GPX4 m6A modification links ferroptosis to NSCLC TKIs resistance2025
  5. 5Ferreting Out Ferroptosis: Extending the Mechanism of Action of RSL3 to the Selenoproteome in Colorectal Cancer2025