摘要
Abstract
Objective To investigate the effect of polyphyllin I on MCF-7 spheroids enriched with cancer stem cells and to preliminarily observe its effect on the hybrid epithelial-mesenchymal transition(EMT)state and its regulatory role on cell stemness.Methods MCF-7 spheroids were cultured under serum-free,non-adherent conditions.Cell viability,invasion,and key protein expression were assessed through the cell counting kit-8 assay,Transwell assay,and Western blot,respectively.The CD44+/CD24-/low cell population was ana-lyzed by flow cytometry.Results The MCF-7 spheroids exhibited high proliferative and invasive capacities,co-expressing the epithelial marker E-cadherin and the mesenchymal marker vimentin,which is indicative of a hybrid EMT state and high stemness.Polyphyllin I treatment significantly suppressed the viability and invasion of MCF-7 spheroids.From a mechanism perspective,polyphyllin I downregulated the E-cadherin/vimentin ratio,significantly reduced the levels of stemness-associated proteins CD44 antigen,aldehyde dehydrogenase 1 family member A1,as well as the ratio of phosphorylated signal transducer and activator of transcription 3 to total signal transducer and activator of transcription 3.Simultaneously,polyphyllin I decreased the proportion of CD44+/CD24-/low cells.No significant changes were observed in key proteins of the intrinsic apoptosis pathway.Conclusions Polyphyllin I reshapes the hybrid EMT state in MCF-7 spheroids,which is accompanied by the disruption of their high stemness equilibrium.This compound may reduce cellular stemness through the EMT re-modeling process,thereby exerting antitumor effects,and this mechanism is independent of the intrinsic apopto-sis pathway.关键词
重楼皂苷Ⅰ/肿瘤干细胞/混合型上皮-间质转化/内源性凋亡Key words
polyphyllin Ⅰ/cancer stem cell/hybrid epithelial-mesenchymal transition/intrinsic apoptosis分类
医药卫生
