Effects of Scutellarin on Gastric Cancer HGC-27 Cells and Its Regulation of Ferroptosis Mechanism
Objective To explore the impact of scutellarin on proliferation,apoptosis,migration,invasion,and ferroptosis processes of gastric cancer HGC-27 cells.Methods Scutellarin was used to intervene with HGC-27 cells.Cell viability was assessed using CCK8,apoptosis was detected by Hochest staining,migration and invasion using scratch assays and Transwell,ROS were measured using DCFH-DA,mitochondrial membrane potential was assessed using JC-1 staining,and Fe2+levels were tested by Ferro Orange.Scutellarin,gastric cancer,and ferroptosis targets were obtained from online databases,and protein-protein interaction analysis was conducted on intersecting targets.Western Blotting was performed to evaluate the expression of EGFR and COX2 after scutellarin intervention.Results The IC50 of scutellarin on HGC-27 cells at 24 h and 48 h were 87.08 pM and 61.69 pM,respectively.Scutellarin significantly induced apoptosis,ROS,mitochondrial membrane potential polarization,Fe2+and COX2 expression levels,while inhibiting scratch healing,migration,invasion,and EGFR expression compared to blank HGC-27 cells,all with statistical significance(P＜0.05).Intersecting targets of scutellarin,gastric cancer,and ferroptosis included EGFR,COX2,MAPK14,HRAS,NOX4,CA9,ALOX5 and KDM5A.Scutellarin effectively reversed the impact of NSC 228155 and rofecoxib on HGC-27 cell viability and Fe2+levels,both statistically significant(P＜0.05).Conclusion Scutellarin demonstrated the ability to inhibit the viability,migration,and invasion of gastric cancer HGC-27 cells,while also inducing apoptosis and ferroptosis in these cells.Notably,scutellarin-induced ferroptosis mechanism is related to its modulation of the EGFR/COX2 signaling pathway.
Scutellaringastric cancer HGC-27ceilsproliferationmigrationinvasionferroptosisEGFR/COX2 signaling pathway
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