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TFEB promotes Ginkgetin-induced ferroptosis via TRIM25 mediated GPX4 lysosomal degradation in EGFR wide-type lung adenocarcinoma

Haojie Wang, Ling-feng Dong, Lili Ding, Xiu-Yuan Miao, Yuwen Zhang, Liping Zhao, Lihua Yu, Zhen-Rong Guan, Ya-Ping Jiang, Xiaoqi Tang, Ya-Xin Yan, Jian-Shu Lou

2025Theranostics15 citationsDOIOpen Access PDF

Abstract

: This study identifies, for the first time, GK as a promising TFEB agonist for LUAD treatment. TFEB activation promotes TRIM25-mediated K48-linked polyubiquitination and lysosomal degradation of GPX4, driving ferroptosis. This ferroptosis-driven mechanism offers a novel strategy to enhance ferroptosis-based anti-LUAD therapies.

Topics & Concepts

TFEBCancer researchAdenocarcinomaAutophagyChemistryLungDegradation (telecommunications)Cell biologyBiologyMedicineCancerInternal medicineBiochemistryApoptosisComputer scienceTelecommunicationsFerroptosis and cancer prognosisRNA modifications and cancerCancer-related molecular mechanisms research
TFEB promotes Ginkgetin-induced ferroptosis via TRIM25 mediated GPX4 lysosomal degradation in EGFR wide-type lung adenocarcinoma | Litcius