ArticleFrontiers in immunology2025
SLC16A3 drives lung adenocarcinoma progression and gefitinib resistance through coordinated regulation of ferroptosis and lactate metabolism.
Article in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Research progress on lactate metabolism in lung cancer: Tumorigenesis, drug resistance and clinical translation (Review).Oncology reports · 2026Review
- Lactylation of β-catenin promotes non-small cell lung cancer by inhibiting ferroptosis through TCF4-mediated GPX4 transcription.Journal of translational medicine · 2026Article
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Authors and funding
7 authors.
Funding
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Abstract
Background: Ferroptosis is an iron-dependent form of regulated cell death that plays a critical role in tumor suppression and therapeutic response. However, the metabolic mechanisms that drive ferroptosis resistance in lung adenocarcinoma (LUAD), particularly in the context of EGFR-TKI tolerance, remain unclear. Methods: We integrated transcriptomic and clinical data from TCGA LUAD cohort and performed survival and enrichment analyses. Functional assays, including proliferation, invasion, ferroptosis indicators, and Results: SLC16A3 expression was elevated in LUAD and was correlated with poor prognosis. SLC16A3 knockdown suppressed tumor cell growth and enhanced ferroptosis, as indicated by increased lipid peroxidation, iron accumulation, and mitochondrial depolarization. Lactate supplementation partially reversed ferroptosis induction. Mechanistically, SLC16A3 was transcriptionally activated by HIF1A, and the HIF1A-SLC16A3 axis conferred ferroptosis resistance and gefitinib tolerance. SLC16A3 inhibition restored ferroptotic sensitivity and enhanced EGFR-TKI efficacy in xenograft models Conclusion: Our findings reveal that the HIF1A-SLC16A3-lactate axis orchestrates ferroptosis suppression and therapeutic resistance in LUAD. Targeting SLC16A3 represents a promising metabolic strategy for overcoming EGFR-TKI resistance by reactivating ferroptosis.
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