中国肿瘤生物治疗杂志2025，Vol.32Issue(3)：281-287,7.DOI:10.3872/j.issn.1007-385x.2025.03.007
圣草次苷通过抑制STAT3/GPX4通路诱导食管癌KYSE30细胞铁死亡
Eriocitrin induces ferroptosis in esophageal cancer KYSE30 cells by inhibiting the STAT3/GPX4 pathway
摘要
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.关键词
食管癌/KYSE30细胞/圣草次苷/铁死亡/活性氧/STAT3/GPX4信号通路Key words
esophageal cancer/KYSE30 cell/Eriocitrin/ferroptosis/reactive oxygen species(ROS)/STAT3/GPX4 signaling pathway分类
医药卫生引用本文复制引用
江蒲,张娜,高坤,靳晶..圣草次苷通过抑制STAT3/GPX4通路诱导食管癌KYSE30细胞铁死亡[J].中国肿瘤生物治疗杂志,2025,32(3):281-287,7.基金项目
河北省自然科学基金(No.H2022206546) （No.H2022206546）
