ArticleTranslational cancer research2025
TFAP2A induces cisplatin resistance via BNIP3-mediated mitophagy in non-small cell lung cancer.
Article in Translational cancer research, 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.
- Comprehensive analysis and validation of the prognostic value of glycosylation- and mitophagy-related genes for head and neck squamous cell carcinoma.Translational cancer research · 2026Article
- Mitochondrial transplant activates CaStem cell research & therapy · 2026Article
- Efficacy and mechanisms of cisplatin and sulforaphane nanoparticles in alleviating cisplatin resistance in non-small cell lung cancer.Translational lung cancer research · 2026Article
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Authors and funding
4 authors.
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Abstract
Background: Cisplatin resistance in non-small cell lung cancer (NSCLC) significantly limits treatment efficacy. Mitophagy has been shown to play a protective role in cisplatin resistance. This study aims to further investigate the mechanisms underlying this process, with a particular focus on identifying transcription factor AP-2 (activating enhancer binding protein 2) alpha (TFAP2A) as a novel regulatory factor in NSCLC. Methods: The correlation between TFAP2A and NSCLC was analysed by The Cancer Genome Atlas (TCGA) database and Kaplan-Meier Plotter database, and validated in clinical samples and cisplatin-resistant NSCLC cells (A549-Re and PC9-Re cells). The changes of mitophagy, apoptosis, and proliferation in cisplatin-resistant NSCLC cells were examined by silencing TFAP2A. The regulatory relationship between TFAP2A and BCL2/adenovirus ElB 19kDa interacting protein 3 (BNIP3) was determined by constructing BNIP3 mutations Results: Our results suggested that TFAP2A might induce cisplatin resistance via BNIP3-mediated mitophagy in NSCLC. The cell counting kit-8 (CCK-8) assay and colony formation showed that silencing TFAP2A dramatically inhibited proliferation and migration of cisplatin-resistant NSCLC cells. The propidium iodide (PI) staining and MitoSOX staining experiments revealed that silencing TFAP2A significantly improved the apoptosis and mitochondrial reactive oxygen species (ROS) levels in cisplatin-resistant NSCLC cells. Subsequently, western blot, reverse transcription quantitative polymerase chain reaction (RT-qPCR) and immunofluorescence experiments revealed that TFAP2A silencing induced cell apoptosis and heightened mitochondrial ROS levels through inhibition of mitophagy via inhibiting BNIP3 pathways. Additionally, western blot, colony formation and immunofluorescence experiments demonstrated that TFAP2A silencing reversed RAPA interventions in cisplatin-resistant NSCLC cells. Finally, we confirmed that TFAP2A silencing can inhibit tumor growth Conclusions: TFAP2A overexpresses significantly in NSCLC, and promotes cisplatin resistance through BNIP3-mediated mitophagy.
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