SLC16A3 drives lung adenocarcinoma progression and gefitinib resistance through coordinated regulation of ferroptosis and lactate metabolism
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.
Authors
- Kai Zhao (ORCID: https://orcid.org/0000-0001-6680-3672)
- Jiamei Jin (ORCID: https://orcid.org/0000-0001-6072-3831)
- Jiaxin Wen (ORCID: https://orcid.org/0000-0001-8660-8866)
- Yiming Liu (ORCID: https://orcid.org/0000-0003-2836-8272)
- Zirui Zhu (ORCID: https://orcid.org/0009-0003-3192-0379)
- Zhiqiang Xue (ORCID: https://orcid.org/0000-0001-9942-3238)
- Wenhan Cai (ORCID: https://orcid.org/0000-0002-8347-4505)
Institutions
- Nankai University (CN)
- Chinese PLA General Hospital (CN)
- Hainan General Hospital (CN)
- Hainan 301 Hospital (CN)
Publication Details
- Journal
- Frontiers in Immunology
- Published
- 2025-11-10
- DOI
- https://doi.org/10.3389/fimmu.2025.1699540
- Primary Topic
- Ferroptosis and cancer prognosis
- Type
- article
- Field-Weighted Citation Impact
- 0.00