机构地区:[1]广西医科大学药学院,南宁530021 [2]省部共建靶向肿瘤学国家重点实验室,南宁530021
出 处:《广西医科大学学报》2024年第6期812-818,共7页Journal of Guangxi Medical University
基 金:国家自然科学基金资助项目(No.81960737,No.82360792)。
摘 要:目的:探讨裂果薯总皂苷(SSPHs)对WB-F344恶性转化细胞上皮间质转化(EMT)及迁移、侵袭的影响及其机制。方法:采用致癌剂1-甲基-3-硝基-1-亚硝基胍(MNNG)体外诱导大鼠肝卵圆细胞系WB-F344制备恶性转化细胞模型。实验分为对照组、MNNG组、MNNG+SSPHs组、MNNG+Wnt-1/β-catenin信号通路激活剂氯化锂(LiCl)+信号通路抑制剂(XAV-939)组、MNNG+LiCl组、MNNG+LiCl+SSPHs组。CCK-8法检测SSPHs对WB-F344恶性转化细胞活力;细胞划痕和Transwell侵袭实验分别检测WB-F344恶性转化细胞的迁移、侵袭能力;蛋白质免疫印迹(western blotting)法检测E-cadherin、N-cadherin、Vimentin、Wnt-1、β-catenin蛋白表达。结果:SSPHs处理后,WB-F344恶性转化细胞活力受到抑制(P<0.05)。与对照组比较,MNNG组划痕愈合率升高,细胞穿膜数增多,N-cadherin、Vimentin、Wnt-1、β-catenin蛋白表达上调,E-cadherin蛋白表达下调(均P<0.05)。与MNNG组比较,MNNG+SSPHs组划痕愈合率降低,穿膜数减少,N-cadherin、Vimentin、Wnt-1、β-catenin蛋白表达下调,E-cadherin蛋白表达上调(均P<0.05)。与MNNG+LiCl组比较,MNNG+LiCl+SSPHs组N-cadherin、Vimentin、Wnt-1、β-catenin蛋白表达下调,E-cadherin蛋白表达上调(均P<0.05),与MNNG+LiCl+XAV-939组结果相同。结论:SSPHs可抑制WB-F344恶性转化细胞的EMT和迁移、侵袭,其机制可能与调控Wnt-1/β-catenin信号通路相关。Objective:To investigate the effect and mechanism of total saponins of Schizocapsa plantaginea Hance(SSPHs)on epithelial mesenchymal transformation(EMT),migration and invasion of WB-F344 malignant transformed cells.Methods:A malignant transformation cell model was prepared by inducing rat hepatic oval cell line WB-F344 in vitro using the carcinogenic agent 1-methyl-3-nitro-1-nitrosoguanidine(MNNG).The experiment was divided into control group,MNNG group,MNNG+SSPHs group,MNNG+Wnt-1/β-catenin signaling pathway activator lithium chloride(LiCl)+signaling pathway inhibitor(XAV-939)group,MNNG+LiCl group,and MNNG+LiCl+SSPHs group.Cell counting kit-8(CCK-8)assay was used to detect the activity of SSPHs on WB-F344 malignant transformed cells;cell scratch assay and Transwell assay were used to detect the migration and invasion ability of WB-F344 malignant transformed cells,respectively.The expression of E-cadherin,N-cadherin,Vimentin,Wnt-1 andβ-catenin proteins was detected by western blotting.Results:After SSPHs treatment,the activity of malignant transformed cells of WB-F344 was inhibited(P<0.05).Compared with the control group,the MNNG group showed an increased scratch healing rate,an increased number of cell membrane penetration,elevated expression levels of N-cadherin,Vimentin,Wnt-1,β-catenin proteins,and a decreased expression level of E-cadherin protein(all P<0.05).Compared with the MNNG group,the MNNG+SSPHs group showed a decrease in scratch healing rate,a decrease number of membrane penetration,down-regulation of N-cadherin,Vimentin,Wnt-1 andβ-catenin protein expression,and up-regulation of E-cadherin protein expression(all P<0.05).Compared with the MNNG+LiCl group,the protein expression of N-cadherin,Vimentin,Wnt-1 andβ-catenin in the MNNG+LiCl+SSPHs group was down-regulated,while the protein expression of E-cadherin was up-regulated(all P<0.05),and the results were the same as those of MNNG+LiCl+XAV-939 group.Conclusion:SSPHs can inhibit EMT,migration and invasion of WB-F344 malignant transformed cells,and
关 键 词:裂果薯总皂苷 Wnt-1/β-catenin信号通路 WB-F344细胞 恶性转化 上皮间质转化 迁移 侵袭
分 类 号:R963[医药卫生—微生物与生化药学]
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