Mechanism of Total Saponins of Clematis on Chemotherapy Resistance of Esophageal Cancer Cells Based on miR-29c/FBXO31 Axis
Objective:To investigate the effect and underlying mechanism of total saponins of clematis(TSC)on the chemotherapy resistance of e-sophageal cancer(EC)Eca109/cDDP cells.Methods:Cell proliferation ability was detected by CCK-8 assay,and the apoptosis level was detected by flow cytometry.Cell migration and invasion abilities were evaluated through Transwell chamber experiments.The target relation-ship was verified by dual-luciferase reporter gene experiments,and the relative expression levels of miR-29c and Fbox31 mRNA were detected by RT-qPCR.Western blot technology was used to measure the relative protein expression of FBXO31,p38 mitogen-activated protein kinase(p38MAPK),p-p38MAPK,caspase-3,and cleaved Caspase-3(C-Caspase-3).Results:The survival rate of Eca109/cDDP cells decreased significantly with increasing concentrations of TSC(P＜0.05).TSC at 10 µg/mL with 0.3 µg/mL cisplatin significantly increased the apop-tosis rate of Eca109/cDDP cells and markedly inhibited cell migration and invasion(P＜0.05).After inhibiting miR-29c expression,cell sur-vival rate,and Fbox31 mRNA and protein relative expression were upregulated,while apoptosis rate,miR-29c relative expression,p-P38MAPK,and C-Caspase-3 protein relative expression were downregulated,and cell migration and invasion significantly increased(P＜0.05).Dual-luciferase reporter gene experiments showed that Fbox31 was the target gene of miR-29c.Conclusion:TSC can enhance the chemotherapy resistance of EC cells,reduce cancer cell survival rate,promote apoptosis,and inhibit migration and invasion.Its mechanism of action may be related to upregulating miR-29c expression,inhibiting Fbox31 expression,and thereby activating the pro-apoptotic program in cancer cells.
Total saponins of clematisEsophageal cancer cellsChemotherapy resistancemicroRNA-29cF-box protein 31
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