摘要
目的分析利多卡因对磷脂酰肌醇3激酶(PI3K)/蛋白激酶B(AKT)信号通路相关蛋白的调控作用,及通过该调控作用对人乳腺癌MCF-7细胞生物学功能的影响。方法将人乳腺癌MCF-7细胞分为对照组、不同剂量(0.5 mM、1 mM和2 mM)利多卡因组及2 mM利多卡因+740Y-P组,采用四甲基偶氮唑蓝法、流式细胞术、Transwell小室法及western blot检测各组细胞增殖、凋亡、迁移和侵袭情况及cl-caspase-3、B淋巴细胞瘤-2(Bcl-2),Bcl-2相关X蛋白(Bax)、基质金属蛋白酶-2(MMP-2)、E-cadherin、PI3K、p-PI3K、Akt、p-Akt蛋白表达。结果与对照组相比,不同剂量利多卡因组MCF-7细胞活力、迁移和侵袭能力、Bcl-2、MMP-2、p-PI3K/PI3K及p-AKT/AKT表达均降低(P<0.05),细胞凋亡率、cl-caspase-3、Bax及E-cadherin蛋白表达均升高(P<0.05),且随着利多卡因剂量的增大,上述指标变化更明显,差异有统计学意义(P<0.05)。与2 mM利多卡因组相比,2 mM利多卡因+740Y-P组MCF-7细胞活力、迁移和侵袭能力、Bcl-2、MMP-2、p-PI3K/PI3K及p-AKT/AKT表达均升高(P<0.05),细胞凋亡率、cl-caspase-3、Bax及E-cadherin蛋白表达均降低,差异有统计学意义(P<0.05)。结论利多卡因可能通过调控PI3K/Akt信号通路抑制人乳腺癌MCF-7细胞的增殖、迁移和侵袭,并促进其凋亡。
Objective To analyze regulatory effects of lidocaine(Lido)on phosphatidylinositol 3 kinase(PI3K)/protein kinase B(AKT)signaling pathway related protein and its influence via this regulatory effects on biological function of human breast cancer MCF-7 cells.Methods MCF-7 cells were divided into control,different Lido doses(0.5 mM,1 mM and 2 mM)and 2 mM Lido+740Y-P group.Cell proliferation,apoptosis,migration and invasion as well as the expression levels of cl-caspase-3,B cell lymphoma-2(Bcl-2),Bcl-2 associated X protein(Bax),matrix metalloproteinase-2(MMP-2),E-cadherin,PI3K,p-PI3K,Akt and p-Akt were analyzed for all groups using methyl thiazolyl tetrazolium(MTT)assay,flow cytometry,Transwell cell method and western blot.Results Compared with control group cell viabilities,migrations and invasion abilities as well as Bcl-2,MMP-2,p-PI3K/PI3K and p-AKT/AKT expression levels lowered(P<0.05)and cell apoptosis rates and the expression levels of cl-caspase-3,Bax and E-cadherin elevated(P<0.05)in different Lido doses groups,above mentioned indexes changed more significantly with the increase of Lido dose,and differences were statistically significant(P<0.05).Compared with 2 mM Lido group cell viability,migration and invasion ability as well as Bcl-2,MMP-2,p-PI3K/PI3K and p-AKT/AKT expression elevated(P<0.05)and cell apoptosis rate and expression levels of cl-caspase-3,Bax and E-cadherin lowered(P<0.05)in 2 mM Lido+740Y-P group,differences were statistically significant(P<0.05).Conclusion Lidocaine may inhibit the proliferation,migration and invasion of MCF-7 cells and promote their apoptosis via regulating PI3K/Akt signaling pathway.
作者
祁向雯
李洪影
刘静
庞红利
Qi Xiangwen;Li Hongying;Liu Jing;Pang Hongli(The First Affiliated Hospital of Henan University,Kaifeng 475000,Henan,China)
出处
《临床心身疾病杂志》
CAS
2023年第6期9-15,共7页
Journal of Clinical Psychosomatic Diseases
基金
开封市科技计划项目(编号2103024)。
关键词
乳腺癌
利多卡因
增殖
凋亡
侵袭
迁移
breast cancer
lidocaine
proliferation
apoptosis
invasion
migration
