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Updated: Sep 9, 2025

Author Spotlight: Tracing the Ferroptotic Signatures and Cell Death Dynamics in Medulloblastoma for Advanced Therapeutics
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Author Spotlight: Tracing the Ferroptotic Signatures and Cell Death Dynamics in Medulloblastoma for Advanced Therapeutics

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SMARCA4欠乏性NSCLCにおけるフェロプトーシス感受性を高めるためにALDH16A1媒介のチオレドキシン分解を標的とする

Guoshu Bi1, Jiaqi Liang1, Yunyi Bian1

  • 1Department of Thoracic Surgery, Zhongshan Hospital, Fudan University, Shanghai, China.

Nature communications
|September 2, 2025
PubMed
まとめ

肺がんにおけるSMARCA4欠乏は,ALDH16A1とチオレドキシン (TXN) を調節することによって,細胞をフェロプトーシスに敏感にします. ALDH16A1の回復またはTXNの抑制は,フェロプトーシス抵抗性がんの化学療法/免疫療法の有効性を高めます.

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The mitochondrial electron transport chain (ETC) is the main energy generation system in the eukaryotic cells. However, mitochondria also produce cytotoxic reactive oxygen species (ROS) due to the large electron flow during oxidative phosphorylation. While Complex I is one of the primary sources of superoxide radicals, ROS production by Complex II is uncommon and may only be observed in cancer cells with mutated complexes.
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After folding, the ER assesses the quality of secretory and membrane proteins. The correctly folded proteins are cleared by the calnexin cycle for transport to their final destination, while misfolded proteins are held back in the ER lumen. The ER chaperones attempt to unfold and refold the misfolded proteins but sometimes fail to achieve the correct native conformation. Such terminally misfolded proteins are then exported to the cytosol by ER-associated degradation or ERAD pathway for...
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