BACKGROUND Abnormal iron metabolism plays a critical role in paclitaxel(PTX)resistance in esophageal cancer cells.Qige San(QG)is a traditional Chinese herbal formula that is reported to improve short-term therapeutic ...BACKGROUND Abnormal iron metabolism plays a critical role in paclitaxel(PTX)resistance in esophageal cancer cells.Qige San(QG)is a traditional Chinese herbal formula that is reported to improve short-term therapeutic effects of esophageal cancer.AIM To investigate the effects and regulatory mechanisms involved in QG-targeted PTX-resistant esophageal cancer cells.METHODS Cell viability was assessed using the Cell Counting Kit-8 assay.Ferroptosis was evaluated by analyzing lipid reactive oxygen species accumulation and the Fe2+concentration in PTX-resistant esophageal cancer cells.Expression of ferroptosis regulators was measured by western blot.Network pharmacology analysis was employed to identify potential targets of QG in PTX-resistant esophageal cancer cells.RESULTS Treatment with QG significantly suppressed the viability,proliferation,and migration of PTX-resistant esophageal cancer cells and simultaneously induced ferroptosis.The network pharmacology analysis identified the phosphoinositide 3-kinase(PI3K)/protein kinase B signaling pathway as the potential target of QG in PTX-resistant esophageal cancer cells.Activation of the PI3K pathway notably reversed the ferroptosis of PTX-resistant esophageal cancer cells that was induced by QG.CONCLUSION QG could repress the resistance of esophageal cancer cells to PTX via targeting the PI3K signaling pathway.展开更多
基金Supported by Zhejiang Traditional Chinese Medicine Administration,No.2024ZL944.
文摘BACKGROUND Abnormal iron metabolism plays a critical role in paclitaxel(PTX)resistance in esophageal cancer cells.Qige San(QG)is a traditional Chinese herbal formula that is reported to improve short-term therapeutic effects of esophageal cancer.AIM To investigate the effects and regulatory mechanisms involved in QG-targeted PTX-resistant esophageal cancer cells.METHODS Cell viability was assessed using the Cell Counting Kit-8 assay.Ferroptosis was evaluated by analyzing lipid reactive oxygen species accumulation and the Fe2+concentration in PTX-resistant esophageal cancer cells.Expression of ferroptosis regulators was measured by western blot.Network pharmacology analysis was employed to identify potential targets of QG in PTX-resistant esophageal cancer cells.RESULTS Treatment with QG significantly suppressed the viability,proliferation,and migration of PTX-resistant esophageal cancer cells and simultaneously induced ferroptosis.The network pharmacology analysis identified the phosphoinositide 3-kinase(PI3K)/protein kinase B signaling pathway as the potential target of QG in PTX-resistant esophageal cancer cells.Activation of the PI3K pathway notably reversed the ferroptosis of PTX-resistant esophageal cancer cells that was induced by QG.CONCLUSION QG could repress the resistance of esophageal cancer cells to PTX via targeting the PI3K signaling pathway.
