临床与实验病理学杂志
臨床與實驗病理學雜誌
림상여실험병이학잡지
CHINESE JOURNAL OF CLINICAL AND EXPERIMENTAL PATHOLOGY
2015年
6期
601-606
,共6页
秦云植%杨洋%朴俊杰%李珍玲%崔雪莲%林贞花
秦雲植%楊洋%樸俊傑%李珍玲%崔雪蓮%林貞花
진운식%양양%박준걸%리진령%최설련%림정화
胃肿瘤%β-拉帕醌%增殖%上皮-间质转化%细胞凋亡
胃腫瘤%β-拉帕醌%增殖%上皮-間質轉化%細胞凋亡
위종류%β-랍파곤%증식%상피-간질전화%세포조망
gastric neop1asms%β-1apachone%pro1iferation%epithe1ia1-mesenchyma1 transition%ce11 apoptosis
目的:探讨β-拉帕醌体外抑制胃癌细胞增殖和迁移及诱导凋亡的作用及机制。方法应用噻唑蓝( MTT)及平板克隆实验检测β-拉帕醌对SGC-7901与AGS胃癌细胞增殖的影响,划痕实验检测β-拉帕醌抑制胃癌细胞的迁移能力,流式细胞术检测β-拉帕醌诱导胃癌细胞凋亡的作用。应用Western b1ot法检测β-拉帕醌处理胃癌细胞前后其增殖、迁移、上皮-间质转化( epithe1ia1-mesenchyma1 transition,EMT)及凋亡分子标志物的变化。结果β-拉帕醌可显著抑制SGC-7901和AGS胃癌细胞的增殖能力,并下调增殖与周期相关Skp2和DEK蛋白的表达( P均<0.05);经β-拉帕醌处理后,胃癌细胞的迁移能力明显下降,且显著下调MMP-2/9和Ezrin蛋白以及EMT间质标志物的表达,上调EMT上皮标志物表达水平;另外,β-拉帕醌增加胃癌细胞的凋亡,下调BCL-2/Bax比值以及上调活化型Caspase-3/8/9的表达。结论β-拉帕醌对胃癌细胞有明显的抑制增殖及诱导凋亡的作用,并可通过MMPs和EMT途径抑制胃癌细胞的迁移能力。
目的:探討β-拉帕醌體外抑製胃癌細胞增殖和遷移及誘導凋亡的作用及機製。方法應用噻唑藍( MTT)及平闆剋隆實驗檢測β-拉帕醌對SGC-7901與AGS胃癌細胞增殖的影響,劃痕實驗檢測β-拉帕醌抑製胃癌細胞的遷移能力,流式細胞術檢測β-拉帕醌誘導胃癌細胞凋亡的作用。應用Western b1ot法檢測β-拉帕醌處理胃癌細胞前後其增殖、遷移、上皮-間質轉化( epithe1ia1-mesenchyma1 transition,EMT)及凋亡分子標誌物的變化。結果β-拉帕醌可顯著抑製SGC-7901和AGS胃癌細胞的增殖能力,併下調增殖與週期相關Skp2和DEK蛋白的錶達( P均<0.05);經β-拉帕醌處理後,胃癌細胞的遷移能力明顯下降,且顯著下調MMP-2/9和Ezrin蛋白以及EMT間質標誌物的錶達,上調EMT上皮標誌物錶達水平;另外,β-拉帕醌增加胃癌細胞的凋亡,下調BCL-2/Bax比值以及上調活化型Caspase-3/8/9的錶達。結論β-拉帕醌對胃癌細胞有明顯的抑製增殖及誘導凋亡的作用,併可通過MMPs和EMT途徑抑製胃癌細胞的遷移能力。
목적:탐토β-랍파곤체외억제위암세포증식화천이급유도조망적작용급궤제。방법응용새서람( MTT)급평판극륭실험검측β-랍파곤대SGC-7901여AGS위암세포증식적영향,화흔실험검측β-랍파곤억제위암세포적천이능력,류식세포술검측β-랍파곤유도위암세포조망적작용。응용Western b1ot법검측β-랍파곤처리위암세포전후기증식、천이、상피-간질전화( epithe1ia1-mesenchyma1 transition,EMT)급조망분자표지물적변화。결과β-랍파곤가현저억제SGC-7901화AGS위암세포적증식능력,병하조증식여주기상관Skp2화DEK단백적표체( P균<0.05);경β-랍파곤처리후,위암세포적천이능력명현하강,차현저하조MMP-2/9화Ezrin단백이급EMT간질표지물적표체,상조EMT상피표지물표체수평;령외,β-랍파곤증가위암세포적조망,하조BCL-2/Bax비치이급상조활화형Caspase-3/8/9적표체。결론β-랍파곤대위암세포유명현적억제증식급유도조망적작용,병가통과MMPs화EMT도경억제위암세포적천이능력。
Purpose To investigate the effects ofβ-1apachone on inhibition of pro1iferation and migration and induction of apoptosis in gastric cancer ce11s in vitro. Methods The ce11 viabi1ity was detected using MTT and co1ony formation assay,the migration abi1ity was determined using scratch assay method,and the apoptosis was examined using f1ow cytometry. Meanwhi1e,the expression of biomarkers of pro1iferation,EMT markers andapoptosiswere detected using Western b1ot ana1ysis. Results β-1apachone cou1d significant1y inhibit the pro1iferation of SGC-7901 and AGS gastric cancer ce11s( P<0. 05),and down-regu1ate the expression 1eve1s of Skp2 and DEK pro-teins. β-1apachonecou1d a1so inhibited the invasion and moti1ity of gastric cancer ce11s via down-regu1ating the expression 1eve1s of MMP-2/9 and Ezrin proteins and up-regu1ating the epithe1ia1 markers. In addition,β-1apachone enhanced the apoptosis of gastric canc-er ce11s,down-regu1ation of BCL-2/Bax ratio and up-regu1ation of activated Caspase-3/8/9. Conclusions β-1apachone can effective1y inhibit the pro1iferation and induce the apoptosis of gastric cancer ce11s,and inhibit the migration of gastric cancer ce11s via MMPs and EMT pathways.