巴伐奇宁调节PI3K/AKT/mTOR信号通路对结直肠癌细胞恶性进展的影响  

Effect of Bavachinin on malignant progression of colorectal cancer cells by regulating the PI3K/AKT/mTOR signaling pathway

作　　者：李伟 江陶 冯雪莉 程吉兵[3] 唐玲[1] LI Wei;JIANG Tao;FENG Xue-li;CHENG Ji-bin;TANG Ling(Department of Pharmacy,Affiliated Hospital of North Sichuan Medical College,Nanchong 637000,Sichuan,China;Department of Orthopedics,Affiliated Hospital of North Sichuan Medical College,Nanchong 637000,Sichuan,China;Department of Clinical Laboratory,Affiliated Hospital of North Sichuan Medical College,Nanchong 637000,Sichuan,China)

机构地区：[1]川北医学院附属医院药剂科,四川南充637000 [2]川北医学院附属医院骨科,四川南充637000 [3]川北医学院附属医院检验科,四川南充637000

出　　处：《川北医学院学报》2024年第3期298-302,315,共6页Journal of North Sichuan Medical College

基　　金：四川省南充市市校科技战略合作专项(20SXQT0101)。

摘　　要：目的:探讨巴伐奇宁(BVC)对结直肠癌细胞恶性进展的影响,分析其与调控磷脂酰肌醇3激酶(PI3K)/蛋白激酶B(AKT)/哺乳动物雷帕霉素靶蛋白(mTOR)信号通路的相关性。方法:将SW480细胞分为对照组(未处理)、低剂量巴伐奇宁组(L-BVC组,10μmol/L)、中剂量巴伐奇宁组(M-BVC组,20μmol/L)、高剂量巴伐奇宁组(H-BVC组,40μmol/L)、Ly294002组(25μmol/L PI3K抑制剂Ly294002)、H-BVC+740Y-P组(40μmol/L BVC和10μmol/L PI3K激活剂740Y-P)。CCK-8法检测SW480细胞增殖情况;流式细胞术检测SW480细胞凋亡情况;划痕实验检测SW480细胞迁移能力;Transwell法检测SW480细胞侵袭能力;Western blot检测细胞中PI3K、AKT、mTOR、p-PI3K、p-AKT、p-mTOR蛋白表达情况。结果:与对照组比较,L-BVC组、M-BVC组、H-BVC组、Ly294002组OD值、划痕愈合率、侵袭细胞数、p-PI3K/PI3K、p-AKT/AKT、p-mTOR/mTOR比值均显著降低(P<0.05),细胞凋亡率显著升高(P<0.05);与H-BVC组比较,H-BVC+740Y-P组OD值、划痕愈合率、侵袭细胞数、p-PI3K/PI3K、p-AKT/AKT、p-mTOR/mTOR比值均显著升高(P<0.05),细胞凋亡率显著降低(P<0.05)。结论:BVC可能通过抑制PI3K/AKT/mTOR信号通路,进而抑制结直肠癌细胞增殖、迁移和侵袭,促进结直肠癌细胞凋亡。Objective:To investigate the impacts of Bavachinin(BVC)on the malignant progression of colorectal cancer cells,and analyze whether its mechanism is related to the regulation of the phosphatidylinositol 3 kinase(PI3K)/protein kinase B(AKT)/mammalian target of rapamycin(mTOR)signaling pathway.Methods:SW480 cells were separated into a control group(untreated),a low-dose Bavachinin group(L-BVC group,10μmol/L),a medium-dose Bavachinin group(M-BVC group,20μmol/L),a high-dose Bavachinin group(H-BVC group,40μmol/L),a Ly294002 group(25μmol/L PI3K inhibitor Ly294002),and an H-BVC+740Y-P group(40μmol/L BVC and 10μmol/L PI3K activator 740Y-P).CCK-8 assay kit was applied to detect SW480 cell proliferation,flow cytometry was applied to detect apoptosis in SW480 cells,scratch experiments were applied to detect SW480 cell migration,Transwell method was applied to detect the invasive ability of SW480 cells,the expression of PI3K,AKT,mTOR,p-PI3K,p-AKT,and p-mTOR proteins in cells was detected by Western blot.Results:Compared with the control group,the OD value,scratch healing rate,number of invasive cells,ratios of p-PI3K/PI3K,p-AKT/AKT,and p-mTOR/mTOR in the L-BVC group,M-BVC group,H-BVC,and Ly294002 group were obviously reduced(P<0.05),the apoptosis rate of cells was obviously increased(P<0.05).Compared with the H-BVC group,the OD value,scratch healing rate,number of invasive cells,ratios of p-PI3K/PI3K,p-AKT/AKT,and p-mTOR/mTOR in the H-BVC+740Y-P group were obviously increased(P<0.05),the apoptosis rate of cells was obviously decreased(P<0.05).Conclusion:BVC may inhibit the PI3K/AKT/mTOR signaling pathway,thereby inhibiting the proliferation,migration,and invasion of colorectal cancer cells,and promoting apoptosis of colorectal cancer cells.

关 键 词：巴伐奇宁 PI3K/AKT/mTOR信号通路 结直肠癌 增殖 凋亡 

分 类 号：R735.37[医药卫生—肿瘤]