ArticleNPJ precision oncology2025
SLC25A39 overexpression exacerbates lung adenocarcinoma progression and is negatively regulated by AFG3L2.
Article in NPJ precision oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- KRAS/ERK2-driven stabilization of AARS1 reprograms tumor metabolism and confers Sorafenib resistance in lung adenocarcinoma.Cell death and differentiation · 2026Article
- SIRT5-dependent desuccinylation licenses UBR5-mediated degradation of TAMM41 to regulate mitochondrial metabolism in lung adenocarcinoma.Biology direct · 2026Article
- Physalin F Promotes AFG3L2-Mediated Degradation of VISA/MAVS to Suppress Innate Immune Response to RNA Virus.Pathogens (Basel, Switzerland) · 2026Article
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Authors and funding
13 authors.
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Abstract
Lung adenocarcinoma (LUAD), the most common lung cancer subtype, has a poor prognosis and limited treatments, underscoring the need for new biomarkers and targets, particularly in mitochondrial metabolism. Our study identifies SLC25A39, a mitochondrial glutathione transporter, as a key oncogenic factor in LUAD. Bioinformatics and tissue analyses revealed significantly elevated SLC25A39 protein levels despite stable mRNA expression, correlating with poorer patient survival. Functionally, SLC25A39 overexpression promoted LUAD cell proliferation and migration, while its knockdown or deletion suppressed these malignant traits in vitro and in vivo. Mechanistically, SLC25A39 loss impaired mitochondrial oxidative phosphorylation, increased reactive oxygen species (ROS), and triggered apoptosis. Notably, we found that reduced expression of the m-AAA protease AFG3L2 in LUAD post-translationally stabilizes SLC25A39, leading to its accumulation. These findings demonstrate that AFG3L2 downregulation drives SLC25A39's oncogenic activity, positioning SLC25A39 as a promising therapeutic target for LUAD.
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Registered trials
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