SLC25A39 overexpression exacerbates lung adenocarcinoma progression and is negatively regulated by AFG3L2.

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. N

SUBMITTER: Hu W 

PROVIDER: S-EPMC12460834 | biostudies-literature | 2025 Sep

REPOSITORIES: biostudies-literature