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Archive > Volume 28 Issue 5 > 2021,28(5):451-459. DOI:10.3872/j.issn.1007-385X.2021.05.005 Prev Next
Basic Research
Fibroblast growth factor 13 regulates apoptosis of A549 cells through the ROS/Caspase-3 pathway
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Abstract:
[Abstract] Objective: To explore the effect of fibroblast growth factor13 (FGF13) on the generation of reactive oxygen species (ROS) and apoptosis of non-small cell lung cancer A549 cells and its regulatory mechanism. Methods: WB was used to detect the background expression of FGF13 in human normal lung epithelial BEAS-2B cells and lung cancer A549 and H460 cells. BEAS-2B and A549 cells were transfected with FGF13 over-expression vector. Two groups of shRNA sequences targeting FGF13 were designed to construct lentivirus interference vector. The packaged lentivirus was used to infect A549 cells. qPCR and WB were used to detect the interference efficiency. DCFH-DA probe combined with fluorescence microplate reader was used to analyze the effect of FGF13 knock-down on the level of ROS in A549 cells. MitoSOX and WB were used to detect mitochondrial ROS levels and nicotinamide adenine dinucleotide phosphate oxidase 4 (NOX4) protein expression levels. Annexin V-FITC-PI double staining method was used to detect the cell apoptosis and expressions of Caspase-3 and Cleaved Caspase-3 protein. Results: FGF13 protein was highly expressed in lung cancer cells compared with BEAS-2B cells (both P<0.05). A549 cell line with over-expression and low-expression of FGF13 were successfully constructed. Over-expression of FGF13 significantly reduced the level of ROS in A549 and BEAS-2B cells (P<0.05), while knockdown of FGF13 significantly increased the level of ROS in A549 cells (P<0.05). Though over-expression and interference of FGF13 had no significant effect on mitochondrial ROS levels in A549 cells, NOX4 protein expression was significantly down-regulated (P<0.05) after FGF13 over-expression and significantly upregulated after FGF13 knockdown (P<0.05), respectively. The interference of FGF13 significantly increased the apoptosis rate (P<0.01) of A549 cells and significantly upregulated the protein expression levels of Caspase-3 and Cleaved Caspase-3 (P<0.05). Conclusion: FGF13 regulates ROS production possibly through the NOX family pathway and regulates apoptosis of A549 cells by the ROS/Caspase-3 pathway.
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Project Supported:
Project supported by the Science and Technology Plan Foundation from Department of Education of Shaanxi Province (No. 20JK0570)
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