消退素D1对结肠癌细胞K-Ras/Notch信号通路串话的影响  

Effect of resolvin D1 on the crosstalk of K-Ras/Notch signaling of colon cancer cells

作　　者：杜恒 吴安定[1] 余洁 王飞 周勇 DU Heng;WU Anding;YU Jie;WANG Fei;ZHOU Yong(Department of Gastrointestinal Surgery,Huanggang Central Hospital,Hubei Province,Huanggang438000,China)

机构地区：[1]湖北省黄冈市中心医院胃肠外科,湖北黄冈438000

出　　处：《中国医药导报》2024年第7期18-22,共5页China Medical Herald

基　　金：湖北省卫生健康委员会科研资助项目(WJ2021M083);湖北省黄冈市市级科技计划资助项目(XQYF2020000018)。

摘　　要：目的 探讨消退素D1(Rv D1)对SW620结肠癌细胞K-Ras/Notch信号通路串话的影响及作用机制。方法 采用CCK-8和克隆形成方法评估Rv D1(0.0、62.5、125.0、250.0、500 nmol/L)对SW620结肠癌细胞短期和长期增殖的影响;将SW620结肠癌细胞分成空白组、Rv D1组、K-Ras组、K-Ras+Rv D1组。空白组不进行处理,K-Ras组和K-Ras+Rv D1组转染K-Ras质粒,Rv D1组和K-Ras+Rv D1组用250 nmol/L的Rv D1处理。蛋白质印迹法检测IL-6、K-Ras、NICD、p-p65、p65、vimentin、N-cadherin和E-cadherin蛋白表达;免疫荧光法检测IL-6、K-Ras和NICD蛋白表达;Transwell实验检测细胞侵袭和迁移水平。结果 125.0、250.0、500.0 nmol/L Rv D1抑制SW620细胞增殖和克隆形成能力(P<0.05)。在Rv D1组中,IL-6、K-Ras、NICD、p-p65、vimentin、N-cadherin蛋白表达均低于空白组,E-cadherin表达高于空白组,差异有统计学意义(P<0.05);K-Ras组的NICD、p-p65、vimentin、N-cadherin的蛋白表达高于空白组,E-cadherin表达低于空白组,差异有统计学意义(P<0.05);K-Ras+Rv D1组的NICD、p-p65、vimentin、N-cadherin表达及细胞侵袭和迁移水平均低于K-Ras组,E-cadherin表达高于K-Ras组,差异有统计学意义(P<0.05)。结论 Rv D1通过抑制IL-6表达,抑制K-Ras对Notch信号通路串话,降低下游核因子-κB水平和上皮-间质转化特性,削弱结肠癌细胞的侵袭转移能力。Objective To investigate the effect of resolvin D1(RvD1)on K-Ras/Notch signaling in SW620 colon cancer cells and its mechanism.Methods The effects of RvD1(0.0,62.5,125.0,250.0,500.0 nmol/L)on the short and long term proliferation of SW620 colon cancer cells were evaluated by CCK-8 and clonal formation methods.SW620 colon cancer cells were divided into blank group,RvD1 group,K-Ras group and K-Ras+RvD1 group.Blank group was not treated,K-Ras group and K-Ras+RvD1 group were transfected with K-Ras plasmid,and RvD1 group and K-Ras+RvD1 group were treated with 250 nmol/L RvD1.The expressions of IL-6,K-Ras,NICD,p-p65,p65,vimentin,N-cadherin,and E-cadherin were detected by Western blot.The expressions of IL-6,K-Ras,and NICD were detected by immunofluorescence.The levels of cell invasion and migration were detected by Transwell assay.Results 125.0,250.0,500.0 nmol/L RvD1 inhibited the proliferation and clonal formation of SW620 cells(P<0.05).The expression of IL-6,K-Ras,NICD,P-P65,vimentin,and N-cadherin in RvD1 group were lower than those in blank group,while the expression of E-cadherin was higher than that in blank group,with statistical significances(P<0.05).The protein expressions of NICD,P-P65,vimentin,and N-cadherin in K-Ras group were higher than those in blank group,and the expression of E-cadherin was lower than that in blank group,with statistical significances(P<0.05).The expression levels of NICD,P-P65,vimentin,and N-cadherin in K-Ras+RvD1 group were lower than those in K-Ras group,and the expression levels of E-cadherin were higher than those in K-Ras group,with statistical significances(P<0.05).Conclusion By inhibiting the expression of IL-6,inhibiting K-Ras cross-talk to Notch signaling pathway,decreasing the downstream nuclear factor-κB level and epithelial-mesenchymal transformation,RvD1 can weaken the invasion and metastasis of colon cancer cells.

关 键 词：消退素D1 结肠癌细胞 串话 RAS NOTCH 

分 类 号：R73-37[医药卫生—肿瘤]