穿心莲内酯抑制胰腺癌SW1990细胞的作用机制  

Mechanism of andrographolide inhibiting proliferation,migration and invasion of pancreatic cancer SW1990 cells

作　　者：徐超[1] 谭小平[1] 李杰 艾明华[1] 刘超勇[1] XU Chao;TAN Xiao-ping;LI Jie;AI Ming-hua;LIU Chao-yong(Department of Gastroenterology,First Hospital of Yangtze University,Jingzhou 434000,Hubei,China)

机构地区：[1]长江大学附属第一医院消化科,荆州434000

出　　处：《医学研究生学报》2022年第7期708-713,共6页Journal of Medical Postgraduates

基　　金：湖北省卫生和计划生育委员会项目资助(WJ2018H204)。

摘　　要：目的胰腺癌治疗上缺乏有效的药物。探讨穿心莲内酯(Ang)对胰腺癌细胞增殖、迁移和侵袭及可能机制。方法体外培养胰腺癌SW1990细胞,分为对照组(常规培养)、Ang(低、中、高剂量)组(分别用15、30、60μmol/LAng作用细胞)、miR-1296-5p组(转染miR-1296-5p模拟物)、miR-NC组(转染模拟对照序列)、Ang+anti-miR-1296-5p(60μmol/LAng作用转染miR-1296-5p抑制剂的细胞)和Ang+anti-miR-NC组(60μmol/LAng作用转染抑制剂阴性序列的细胞),CCK-8法、克隆形成实验、划痕实验和Transwell分别检测细胞增殖抑制率、克隆形成形成能力、迁移及侵袭,蛋白质印迹法检测细胞中E-cadherin和N-cadherin蛋白表达,qRT-PCR法检测细胞中miR-1296-5p表达。结果与对照组比较,Ang(低、中、高剂量)组细胞抑制率、E-cadherin蛋白和miR-1296-5p表达量均升高(P<0.05),细胞克隆形成数、划痕愈合率、侵袭数及N-cadherin蛋白表达量均降低(P<0.05)。miR-1296-5p组细胞抑制率[(46.18±4.49)%]较miR-NC组[(6.11±0.42)%]升高(P<0.05)、E-cadherin蛋白表达量亦升高(P<0.05),细胞克隆形成数[(53.58±5.29)个]、划痕愈合率[(31.58±3.16)%]、侵袭数[(64.11±5.64)个]较miR-NC组[(106.03±10.08)个、(72.69±5.13)%、(127.38±10.89)个]明显降低(P<0.05)且N-cadherin蛋白表达量亦降低(P<0.05)。抑制miR-1296-5p逆转了Ang对SW1990细胞增殖、迁移和侵袭的影响。结论Ang可能通过上调miR-1296-5p抑制胰腺癌SW1990细胞增殖、迁移和侵袭,具有治疗胰腺癌的潜在价值。Objective There is a lack of effective drugs to treat pancreatic cancer.To investigate the effect of andrographolide(Ang)on proliferation,migration and invasion of pancreatic cancer cells and its possible mechanism.Methods Pancreatic cancer SW1990 cells were cultured in vitro and divided into control group(conventional culture),Ang(low,medium and high doses)groups(15,30,and 60μmol/L Ang were used to act on cells,respectively),miR-1296-5p group(transfected with miR-1296-5p simulators),miR-NC group(transfected with simulated control sequences),Ang+anti-miR-1296-5p(cells transfected with miR-1296-5p inhibitor were treated with 60μmol/L Ang)and Ang+anti-miR-NC group(cells transfected with inhibitor-negative sequences were treated with 60μmol/L Ang).CCK-8 method,clone formation test,scratch test and Transwell were used to detect cell proliferation inhibition rate,clonogenesis ability,migration and invasion,respectively.The protein expression of E-cadherin and N-cadherin in cells was detected by Western blotting,and the expression of miR-1296-5p was detected by qRT-PCR.Results Compared with the control group,the cell inhibition rate,the expression of E-cadherin protein and miR-1296-5p were increased in Ang(low,medium and high dose)groups(P<0.05),and the number of cell clone formation,the rate of wound healing,the number of invasion and the expression of N-cadherin protein were decreased in Ang(low,medium and high dose)groups(P<0.05).The cell inhibition rate of miR-1296-5p group[(46.18±4.49)%]was higher than that of miR-NC group[(6.11±0.42)%](P<0.05),and the expression of E-cadherin protein was also increased(P<0.05).The number of cell clones[(53.58±5.29)],the rate of scratch healing[(31.58±3.16)%],the number of invasion[(64.11±5.64)]significantly decreased compared with miR-NC group[(106.03±10.08),(72.69±5.13)%,(127.38±10.89)](P<0.05),and N-cadherin protein expression was also decreased(P<0.05).Inhibition of miR-1296-5p reversed the effects of Ang on proliferation,migration and invasion of SW1990 cells.Concl

关 键 词：穿心莲内酯 胰腺癌 miR-1296-5p 细胞增殖 侵袭 

分 类 号：R735.9[医药卫生—肿瘤]