ArticleMolecular genetics and genomics : MGG2026
USP11 inhibits cuproptosis in non-small cell lung cancer by deubiquitinating IGF2BP2 to enhance the stability of m6A-modified ATOX1 mRNA.
Article in Molecular genetics and genomics : MGG, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Inducing cuproptosis is considered a novel strategy to impede non-small cell lung cancer (NSCLC) progression. ATOX1 suppressed cuproptosis by chelating free copper ions. This study seeks to elucidate the pathways that regulate ATOX1 upstream and thereby pinpoint molecular targets for activating cuproptosis in NSCLC. Cuproptosis was induced with ES-Cu. Malignant phenotypes were assessed using CCK-8, clonogenic, and Transwell assays. RNA immunoprecipitation, RNA pull-down, and actinomycin D chase were used to examine IGF2BP2-ATOX1 mRNA interaction and mRNA stability. Protein-protein interactions and ubiquitination were examined by co-immunoprecipitation. The co-localization of USP11 and IGF2BP2 was visualized by immunofluorescence. IGF2BP2 protein stability was assessed following cycloheximide treatment. Copper content was quantified using a commercial kit. Gene and protein levels were evaluated by RT-qPCR and Western blot. RNA-binding domain mutant rescue experiments were conducted to determine the functional requirement of IGF2BP2 KH domains. A subcutaneous xenograft model was established to validate the regulatory axis in vivo. ATOX1 suppressed cuproptosis to support NSCLC proliferation. IGF2BP2 bound to the CDS of ATOX1 mRNA via the m6A site at position 261, thereby enhancing ATOX1 mRNA stability. The KH3-4 domains of IGF2BP2 were indispensable for this regulation. Upregulation of ATOX1 by IGF2BP2 inhibited cuproptosis and consequently drove NSCLC proliferation. USP11 maintained IGF2BP2 protein stability via deubiquitination, leading to suppression of cuproptosis and promotion of NSCLC progression through the IGF2BP2/ATOX1 axis in vitro. In vivo, the USP11-IGF2BP2-ATOX1 axis might promote NSCLC tumor growth by suppressing cuproptosis. USP11‑dependent deubiquitination stabilized IGF2BP2, which subsequently increased ATOX1 mRNA stability in an m6A‑dependent manner. Elevated ATOX1 expression inhibited cuproptosis and thereby accelerated NSCLC progression.
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