沙苑子苷A下调NF-кB信号通路抑制卵巢癌细胞恶性表型的研究  

Study on Complanatoside A downregulating nuclear factor-KB signaling to suppress the malignant phenotype of ovarian cancer cells

作　　者：宋慧 贾文娟[2] SONG Hui;JIA Wenjuan(Department of Traditional Chinese Medicine Gynecology,Huainan Maternal and Child Health Hospital,Huainan 232001,Anhui,China;Department of Gynecology,Huainan Maternal and Child Health Hospital,Huainan 232001,Anhui,China)

机构地区：[1]淮南市妇幼保健院中医妇科,安徽淮南232001 [2]淮南市妇幼保健院妇科,安徽淮南232001

出　　处：《中国性科学》2023年第12期81-86,共6页Chinese Journal of Human Sexuality

基　　金：2021年度淮南市指导性科技计划项目(2021084)。

摘　　要：目的 探究沙苑子苷A调控核因子-κB(NF-κB)信号通路对人卵巢癌细胞克隆、黏附及侵袭的影响。方法 体外培养人卵巢癌Caov3细胞,分为对照组(不做干预)及25、50、100、200μg/mL沙苑子苷A组。采用细胞计数试剂盒-8(CCK-8)测定细胞活力筛选实验浓度,而后将Caov3细胞分为对照组、实验组(100μg/mL沙苑子苷A)、阳性药物组(100 nmol/L紫杉醇)、激活剂组(100μg/mL沙苑子苷A+1μmol/L NF-κB通路激活剂PMA)和抑制剂组(100μg/mL沙苑子苷A+5μmol/L NF-κB通路抑制剂BAY 11-7082),干预24 h。采用平板克隆形成、细胞黏附、Transwell小室、蛋白免疫印迹(WB)法对细胞克隆形成率、黏附数、侵袭数、细胞周期蛋白D1(Cyclin D1)、增殖细胞核抗原(PCNA)和NF-κB信号通路相关蛋白进行分析。结果 与对照组相比,50、100、200μg/mL沙苑子苷A组细胞活力降低(P<0.05),选择细胞活力接近50%的100μg/mL沙苑子苷进行后续实验。与对照组相比,实验组和阳性药物组细胞克隆形成率、黏附数、侵袭数及Cyclin D1、PCNA、p-IκBα、p-NF-κB p65蛋白表达量显著降低(P<0.05)。与实验组相比,BAY 11-7082可增强沙苑子苷A对细胞上述指标的作用,PMA可削弱沙苑子苷A对细胞上述指标的作用(P<0.05)。结论 沙苑子苷A可通过阻断NF-κB通路抑制人卵巢癌Caov3细胞的克隆、黏附、侵袭。Objective To explore the effects of Complanatoside A regulating nuclear factor-κB(NF-κB)signal pathways on the cloning,adhesion and invasion of ovarian cancer cells.Methods Human ovarian cancer Caov3 cells were cultured in vitro and divided into control group(without intervention),25,50,100,200μg/mL Complanatoside A group,cell viability was determined with cell counting kit-8(CCK-8)to screen the appropriate concentration for subsequent experiments.Then Caov3 cells were divided into control group,experimental group(100μg/mL Complanatoside A),positive control group(100 nmol/L paclitaxel),activator group(100μg/mL Complanatoside A+1μmol/L NF-κB pathway activator PMA)and inhibitor group(100μg/mL Complanatoside A+5μmol/L NF-κB pathway inhibitor BAY 11-7082)for 24 hours.Clonogenic assay in plates,cell adhesion assay,Transwell chambers,and Western blot(WB)analysis were performed to evaluate the clonogenic rate,adhesion,invasion,cyclin D1,proliferating cell nuclear antigen(PCNA)and NF-κB signaling pathway related protein expression levels.Results Compared with the control group,the cell viability of 50,100,200μg/mL Complanatoside A group decreased(P<0.05).The viability of 100μg/mL Complanatoside A cells with cell activity close to 50%was selected for follow-up experiment.Compared with the control group,the cell clonogenic rate,adhesion number,invasion number,and the expression of cyclin D1,PCNA,p-IκBαand p-NF-κB p65 protein in the experimental group and the positive control group decreased(P<0.05).Compared with the experimental group,BAY 11-7082 enhanced and PMA weakened the effects of Complanatoside A on the above indices(P<0.05).Conclusions Complanatoside A could inhibit the cloning,adhesion and invasion of Caov3 cells of human ovarian cancer by blocking NF-κB pathway.

关 键 词：卵巢癌 沙苑子苷A 核因子-ΚB信号通路 克隆 黏附 侵袭 

分 类 号：R711[医药卫生—妇产科学]