Effects of hispidulin on the proliferation,invasion and epithelial mesenchymal transition of breast cancer cells by regulating the NF-κB and PI3K/AKT signaling pathways
CHENG Chao
WANG Zhou
ZHANG Weiqun
Abstract：Objective To investigate the effects of hispidulin(His)on the proliferation,invasion and epithelial mesenchymal transition of breast cancer cells by regulating the nuclear factor kappa-B(NF-κB)and phosphatidylinositol 3-kinase(PI3K)/protein kinase B(AKT)signaling pathway.Methods Breast cancer cells MCF-7 were induced with blank control,low-dose His(5 μmol/L),medium-dose His(10 μmol/L),high-dose His(20 μmol/L),and high-dose His+the PI3K activator 740Y-P(10 μmol/L).Cell proliferation,apoptosis,migration and invasion were detected by cell counting kit-8(CCK-8)assay,flow cytometry,wound healing assay and Transwell assay,respectively.Western blot was applied to detect the protein expressions of E-cadherin,N-cadherin,Snail,NF-κB p65,PI3K,p-PI3K,AKT,and p-AKT.Results Compared with those of blank control,MCF-7 cells induced with low-dose,medium-dose and high-dose His showed significantly lower optical density(OD)value,wound healing rate,number of invasive cells,protein expressions of N-cadherin,Snail and NF-κB p65,p-PI3K/PI3K and p-AKT/AKT,but higher apoptotic rate and protein expression of E-cadherin(P＜0.05).Compared with those induced with high-dose His,MCF-7 cells induced with high-dose His+740Y-P showed significantly higher OD value,wound healing rate,number of invasive cells,protein expressions of N-cadherin,Snail and NF-κB p65,p-PI3K/PI3K and p-AKT/AKT,but lower apoptotic rate and protein expression of E-cadherin(P＜0.05).Conclusion His can inhibit the NF-κB and PI3K/Akt signaling pathways,and further inhibit the proliferation,invasion and epithelial mesenchymal transition of breast cancer cells,and promote their apoptosis.
Keywords：hispidulinnuclear factor kappa-Bphosphatidylinositol 3 kinase/protein kinase B signaling pathwaybreast cancerproliferationinvasionepithelial mesenchymal transition
Publication Date：2025-10-26
Online Publishing Date：2025-11-19(First online date of this platform, not the publication date of the document)
Pages：5( 1617-1621 )