التفاصيل البيبلوغرافية
| العنوان: |
SNX30 inhibits lung adenocarcinoma cell proliferation and induces cell ferroptosis through regulating SETDB1. |
| المؤلفون: |
Fan, Xinjie1 (AUTHOR) fxj14391228@163.com, Zhu, Qichu1 (AUTHOR), Du, Chengzhuo1 (AUTHOR), Chen, Jinlai1 (AUTHOR), Su, Yingming1 (AUTHOR) |
| المصدر: |
Journal of Cardiothoracic Surgery. 1/9/2025, Vol. 20 Issue 1, p1-10. 10p. |
| مصطلحات موضوعية: |
*REACTIVE oxygen species, *GLUTATHIONE peroxidase, *LUNG cancer, *GENETIC transcription, *WESTERN immunoblotting |
| مستخلص: |
Background: Lung adenocarcinoma is the most common form of lung cancer and one of the most life-threatening malignant tumors. Ferroptosis is an iron-dependent regulatory cell death pathway that is crucial for tumor growth. SNX30 is a key regulatory factor in cardiac development; however, its regulatory mechanism and role in inducing ferroptosis in lung adenocarcinoma remain unclear. Objective: This study aimed to elucidate the functions and specific mechanisms of action of SNX30 in lung adenocarcinomas. Methods: SNX30 levels in lung adenocarcinoma cell lines (A549 and HCC827) were determined using reverse transcription quantitative real-time PCR (RT-qPCR) or western blotting. Cell proliferation and apoptosis were assessed by CCK8 and flow cytometry, respectively. The intracellular levels of total iron and Fe2+ were detected using Iron Assay Kits. Reactive oxygen species (ROS) levels were evaluated using a DCFH-DA probe and flow cytometry. Cysteine (Cys), glutathione (GSH), and glutathione peroxidase 4 (GPX4) levels were measured using detection assay kits. Other related markers, including Ptgs2, Chac1, SETDB1 cleaved-Caspase3, and Caspase3 were analyzed by RT-qPCR or western blotting. Results: SNX30 is downregulated in lung adenocarcinoma cell lines. SNX30-plasmid depressed lung adenocarcinoma cell proliferation, accelerated apoptosis, enhanced cleaved-Caspase3 expression and cleaved-Caspase3/Caspase3 ratio. Ferrostatin-1 significantly reversed the effects of the SNX30-plasmid on cell ferroptosis in lung adenocarcinoma, as confirmed by the reduced ROS levels, inhibited intracellular total iron and Fe2+ levels, decreased Ptgs2 and Chac1 expression, and increased Cys, GSH, and GPX4 release. We observed that the level of SETDB1 was lower in the SNX30-plasmid group than in the control-plasmid group, whereas the opposite results in ferrostatin-1 treated cells. SNX30 negatively regulates SETDB1 expression in lung adenocarcinoma cells. The upregulation of SETDB1 reversed the effects of the SNX30-plasmid on ferroptosis in lung adenocarcinoma cells. Conclusion: SNX30 inhibits lung adenocarcinoma cell proliferation and induces ferroptosis by regulating SETDB1 expression. [ABSTRACT FROM AUTHOR] |
| قاعدة البيانات: |
Academic Search Index |
Full Text Finder