Erianin inhibits the proliferation of esophageal cancer cells through TNF-α signaling pathway
In order to explore the effects of erianin on the proliferation of esophageal cancer cells through TNF-α signaling path-way,network pharmacological analysis was used to identify the target of erianin against esophageal cancer.Esophageal cancer cells EC109 and KYSE510 were treated with different concentrations of erianin(0,15,30,45,60 nmol/L),and cell prolifera-tion was detected by CCK-8 and clone formation assays.Nude mice were used to construct the esophageal cancer model.The expression of Ki67 protein in tumor tissue was detected and expressions of TNF-α and its downstream pathway related proteins were examined by Western blotting.The expression of TNF-α in esophageal cancer and its effects on cell proliferation were analyzed by bioinformatics.The results showed that TNF-α was the Top1 gene in the anti-esophageal cancer target of erianin.Compared to those of the 0 nmol/L erianin group,the cell proliferation rates of EC109 and KYSE510,clone formation rate,and expression levels of phosphorylated(p)-NF-κB p65,p-MAPK,p-JNK,and TNF-α protein were significantly decreased after treatment with erianin(15,30,45,60 nmol/L,P＜0.05).Compared to those of the control group,the volume and mass of tumors,and expression of Ki67 protein in the erianin-treated tumor tissue were significantly decreased(P＜0.05).The expression of TNF-α was up-regulated in esophageal cancer.The gene sets related to cell proliferation and cycle were significantly enriched in TNF-α high-expression group,while the gene sets related to apoptosis were significantly enriched in TNF-α low-expression group.After treatment with TNF-α,cell viability and proliferation of EC109 and KYSE510 were significantly increased(P＜0.05)and the phenomenon that erianin inhibited the activation of NF-κB signaling pathway was significantly reversed.This study concludes that erianin can inhibit the proliferation of esophageal cancer cells and the growth of transplanted tumors by inhibiting the TNF-α and its downstream signaling pathway.
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