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Archive > Volume 32 Issue 3 > 2025,32(3):281-287. DOI:10.3872/j.issn.1007-385X.2025.03.007 Prev Next
Basic Research
Eriocitrin induces ferroptosis in esophageal cancer KYSE30 cells by inhibiting the STAT3/GPX4 pathway
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Abstract:
[Abstract] Objective: To investigate the effect of Eriocitrin on the proliferation of esophageal cancer KYSE30 cells, and to explore its possible mechanism based on ferroptosis. Methods: Esophageal cancer KYSE30 cells were divided into 8 groups: the control group (conventional culture), RSL3 group (treated with 3 μmol/L ferroptosis inducer RSL3), Eriocitrin group (treated with 75 μmol/L Eriocitrin), Eriocitrin + Fer-1 group (treated with 5 μmol/L of ferroptosis inhibitor Fer-1 and 75 μmol/L Eriocitrin), Fer-1 group (treated with 5 μmol/L Fer-1 treatment), oe-NC group (transfected with blank vector control), oe-STAT3 group (transfected with STAT3 overexpression vector) and oe-STAT3 + Eriocitrin group (transfected with STAT3 overexpression vector and then treated with 75 μmol/L Eriocitrin). Proliferation abilities of cells in each group were detected using CCK-8 assay, EdU incorporation assay and clone formation assay respectively. The levels of intracellular ferroptosis-related indicators were detected using the ELISA kits. Western blotting was used to detect the expression of STAT3/GPX4 pathway-related proteins. KYSE30 cell nude mouse subcutaneous transplanted tumor model was constructed to observe the effects of Eriocitrin and Fer-1 on the growth of transplanted tumors. Results: Eriodictyol could inhibit the proliferation and clone formation of KYSE30 cells, increase the levels of reactive oxygen species (ROS), malondialdehyde (MDA) and Fe2+, decrease the level of glutathione (GSH) (all P < 0.05) and suppress the growth of transplanted tumors in nude mice. These effects could be reversed by Fer-1 (P < 0.05). Overexpression of STAT3 could abolish the inductive effect of eriodictyol on ferroptosis and its inhibitory effect on the STAT3/GPX4 pathway (P < 0.05). Conclusion: Eriocitrin could induce ferroptosis in esophageal cancer KYSE30 cells by inhibiting STAT3/GPX4 signaling pathway and exert significant antitumor effects in esophageal cancer.
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