摘要
目的探究甘草查尔酮B对胃癌SGC-7901细胞生物学行为的影响。方法SGC-7901细胞分为4组:对照组、40、80、120 txm ol/L甘草查尔酮B剂量组。CCK-8和克隆形成实验检测细胞增殖;流式检测细胞凋亡;Transw ell检测细胞侵袭;体外成管实验检测微管形成;免疫荧光检测A K T膜定位;W estern印迹检测相关蛋白表达。结果中、高剂量甘草查尔酮B可抑制细胞的增殖、侵袭、微管形成数及间质细胞形态,并促进凋亡。中、高剂量甘草查尔酮B可上调p 53表达,下调K i67、VEGF、p-P13K、p-AKT表达,并减少AKT细胞膜定位。结论甘草查尔酮B可抑制SGC-7901细胞增殖、侵袭,促进凋亡,并抑制微管形成和PI3K/AKT通路活性。
Objective To explore the effects of licochalcone B on the biological behaviors of gastric cancer SGC-7901 cells.Methods SGC-7901 cells were divided into 4 groups:control group,40,80 and 120 mol/L licochalcone B groups.Cell proliferation was detected by CCK-8 and clonal formation assay,apoptosis by flow cytometry,and cell invasion by Transwell assay.The formation of microtubules was observed in vitro.Immunofluorescence assay was used to detect membrane localization of(AKT),and Western blotting to measure the expression of related proteins.Results Medium and high doses of licochalcone B inhibited cell proliferation,invasion,microtubule formation and mesenchymal cell morphology,and promoted apoptosis.They could up-regulate the expression of p53,down-regulate the expression of Ki67,VEGF,P-PI3K and P-Akt,and reduce the membrane localization of AKT.Conclusion Licochalcone B can inhibit the proliferation and invasion of SGC-7901 cells,promote apoptosis,and inhibit microtubule formation and activity of PI3K/AKT pathway.
作者
杨娟
唐燕君
YANG Juan;TANG Yanjun(Pharmacy Department,Affiliated Hospital of North Sichuan Medical College,Nanchong,Shichuan,637000,China;Pharmacy department,West China Hospital of Sichuan University,Chengdu,610041,China)
出处
《医学分子生物学杂志》
CAS
2020年第3期228-233,共6页
Journal of Medical Molecular Biology
基金
四川省卫计委重点课题(NO.18ZD023)。
关键词
甘草查尔酮B
胃癌
增殖
侵袭
凋亡
Licochalcone B
gastric cancer
proliferation
invasion
apoptosis
