Qige San regulates paclitaxel resistance in esophageal cancer by targeting ferroptosis

Figure 1 Qige San regulated paclitaxel resistance in esophageal cancer. A: The viability of TE-1/paclitaxel (PTX) and EC109/PTX and parental cancer cells treated with PTX; B: Viability of TE-1/PTX and EC109/PTX cells that treated with PTX and Qige San (QG); C: Proliferation of TE-1/PTX and EC109/PTX cells that treated with PTX and QG; D: Migration of TE-1/PTX and EC109/PTX cells that treated with PTX and QG. Data are mean ± standard error of the mean (n = 3). ^aP < 0.05; ^cP < 0.001 vs control; ^fP < 0.001 vs QG (one-way analysis of variance with Tukey’s test); QG: Qige San; PTX: Paclitaxel; Cont: Control.

Figure 2 Qige San regulates ferroptosis in esophageal cancer. A: Level of total iron; B: Level of Fe²⁺; C: Level of malondialdehyde; D: Protein expression of glutathione peroxidase 4 and SLC7A11. Data are mean ± standard error of the mean (n = 3). ^cP < 0.001 vs control; ^fP < 0.001 vs Qige San (one-way analysis of variance with Tukey’s test); QG: Qige San; PTX: Paclitaxel; Cont: Control; MDA: Malondialdehyde; GPX4: Glutathione peroxidase 4.

Figure 3 Network pharmacological analysis of potential targeted signaling pathways of Qige San in esophageal cancer. A: Active compounds and target genes identified by Traditional Chinese Medicine Systems Pharmacology database; B: Overlapped genes of disease targets from GeneCards, Therapeutic Target Database, and Online Mendelian Inheritance in Man database; C: Overlapped genes of disease targets and drug targets; D: Gene Ontology analysis of the overlapped genes; E: Kyoto Encyclopedia of Genes and Genomes analysis of the overlapped genes; F: HALLMARK analysis of the overlapped genes; G: REACTOME analysis of the overlapped genes; H: Protein-protein interaction analysis of the overlapped genes; I: Gene Ontology analysis of the connected genes; J: Kyoto Encyclopedia of Genes and Genomes analysis of the connected genes; K: HALLMARK analysis of the connected genes; L: REACTOME analysis of the connected genes.

Figure 4 Qige San regulated paclitaxel resistance in esophageal cancer cells by targeting ferroptosis through the Akt signaling pathway. A: Cell viability was detected by the Cell Counting Kit-8; B: Cell proliferation measured by colony formation assay; C and D: Total iron and Fe²⁺ level in paclitaxel-resistant esophageal cancer cells; E: Malondialdehyde production in paclitaxel-resistant esophageal cancer cells; F: Protein expression of glutathione peroxidase 4 and SLC7A11. Data are mean ± standard error of the mean (n = 3). ^cP < 0.001 vs control; ^fP < 0.001 vs Qige San (one-way analysis of variance with Tukey’s test); QG: Qige San; PTX: Paclitaxel; Cont: Control; MDA: Malondialdehyde; Fer-1: Ferroptosis inhibitor; act: PI3K activator; GPX4: Glutathione peroxidase 4.