中国肿瘤生物治疗杂志2025，Vol.32Issue(6)：604-610,7.DOI:10.3872/j.issn.1007-385x.2025.06.006
花旗松素通过Rac1/NF-κB/AKT信号通路抑制膀胱癌T24细胞的恶性生物学行为
Toxifolin inhibits malignant biological behaviors of bladder cancer T24 cells via Rac1/NF-κB/AKT signaling pathway
摘要
Abstract
Objective:To investigate the effect of toxifolin(TAX)on the malignant biological behaviors of human bladder cancer T24 cells through the Rac1/NF-κB/AKT signaling pathway.Methods:Bladder cancer T24 cells were routinely cultured and divided into:Ctrl group(untreated),TAX-L group(5 μmol/L TAX),TAX-M group(10 μmol/L TAX),TAX-H group(20 μmol/L TAX),and TAX-H+Rac1 activator group(20 μmol/L TAX+50 nmol/L ML-097).CCK-8 method,clone formation assay,scratch healing assay,Transwell chamber assay,and flow cytometry were used to evaluate the effects of different concentrations of TAX on the proliferation,migration,invasion,and apoptosis of T24 cells.WB method was used to examine the expression of apoptosis-related proteins,epithelial-mesenchymal transition(EMT)-related proteins,and Rac1/NF-κB/AKT axis related proteins in T24 cells;A nude mice xenograft model was used to assess the effect of TAX on tumor growth.Results:TAX dose-dependently inhibited the proliferation,migration,and invasion of T24 cells and promoted apoptosis(all P<0.05).TAX also increased the expression of apoptosis proteins BAX and E-cadherin,while decreasing the expression of Bcl-2,N-cadherin,and Rac1/NF-κB/AKT signaling pathway-related proteins(all P<0.05).Furthermore,TAX inhibited tumor growth in the xenograft model(P<0.05).ML-097 partially reversed these effects(all P<0.05).Conclusion:TAX inhibits the malignant biological behaviors of bladder cancer T24 cells and promotes their apoptosis by inhibiting Rac1/NF-κB/AKT signaling pathway.关键词
花旗松素/Rac1/NF-κB/AKT信号通路/膀胱癌/T24细胞/恶性生物学行为Key words
toxifolin(TAX)/Rac1/NF-κB/AKT signaling pathway/bladder cancer/T24 cell/malignant biological behavior分类
医药卫生引用本文复制引用
路通,元晓科,付天英,邵永刚,路英文..花旗松素通过Rac1/NF-κB/AKT信号通路抑制膀胱癌T24细胞的恶性生物学行为[J].中国肿瘤生物治疗杂志,2025,32(6):604-610,7.基金项目
河北省医学科学研究课题计划(No.20220216) （No.20220216）
