ArticleCell death & disease2025
TFIIB-related factor 2 inhibits lung squamous carcinoma cell apoptosis through SLC8A3-mediated mitochondrial homeostasis.
Article in Cell death & disease, 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.
- PINK1 promotes the progression of lung squamous cell carcinoma through the FAK/AKT/RhoA/vinculin pathway.Oncology reports · 2026Article
- Different forms of cardiomyocyte death in post-myocardial infarction ventricular remodeling: mechanisms and therapeutic strategies.Frontiers in cardiovascular medicine · 2026Review
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Authors and funding
10 authors.
Funding
Abstract
Lung cancer is the most common cancer and the leading cause of cancer-related deaths. Developing therapies for lung cancer is challenging, and new targets are urgently required. TFIIB-related factor 2 (BRF2) plays a crucial role in the development and progression of various tumors. However, the potential role of BRF2 in lung squamous carcinoma (LUSC) is unclear. Therefore, the aim of this study was to elucidate the mechanism of BRF2 regulation in LUSC development. Flow cytometry, protein blotting, and in vivo experiments were performed to assess the function of BRF2 in LUSC. Transmission electron microscopy imaging and mitochondrial membrane potential (MMP) measurements were used to determine the effect of BRF2 on mitochondria in LUSC. The impact of the downstream molecule SLC8A3 was predicted using bioinformatics analysis, and the mechanism was investigated by analyzing quantitative reverse transcription-polymerase chain reaction and immunoprecipitation (IP) assays, which were confirmed through rescue experiments. BRF2 expression was upregulated in squamous carcinoma cells, which increased SLC8A3 protein expression, promoted mitochondrial autophagy, stabilized MMP, and reduced apoptosis. In addition, SLC8A3 overexpression inhibited PTEN-induced putative kinase 1 (PINK1) binding to TIMM23 to promote mitochondrial autophagy and stabilize the MMP, which counteracted BRF2 knockdown-induced apoptosis. BRF2 mediated SLC8A3 expression to reduce apoptosis in LUSC cells by maintaining mitochondrial homeostasis. These findings provide novel selective therapeutic targets and ideas for the treatment of LUSC.
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