[1]彭琬昕,万燕雅,葛璐,等.siRNA干扰即刻早期基因Egr-1对汉防己甲素诱导的胰腺癌细胞自噬、凋亡的作用研究[J].南京师范大学学报(自然科学版),2015,38(03):71.
 PengWanxin,WanYanya,GeLu,et al.EffectofRNAInterferenceTargetingEgr-1InhibiteTetrandrine-InducedAutophagyandApoptosisofPancreaticPaTu8988Cellsinvitro[J].Journal of Nanjing Normal University(Natural Science Edition),2015,38(03):71.
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siRNA干扰即刻早期基因Egr-1对汉防己甲素诱导的胰腺癌细胞自噬、凋亡的作用研究()
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《南京师范大学学报》(自然科学版)[ISSN:1001-4616/CN:32-1239/N]

卷:
第38卷
期数:
2015年03期
页码:
71
栏目:
生命科学
出版日期:
2015-09-30

文章信息/Info

Title:
EffectofRNAInterferenceTargetingEgr-1InhibiteTetrandrine-InducedAutophagyandApoptosisofPancreaticPaTu8988Cellsinvitro
作者:
彭琬昕1万燕雅2葛璐1金洁1龚爱华1吴朝阳2
(1.江苏大学医学院生物系,江苏镇江212013)
(2.江苏大学附属人民医院肿瘤放疗科,江苏镇江212013)
Author(s):
PengWanxin1WanYanya2GeLu1JinJie1GongAihua1WuChaoyang2
(1.DepartmentofBiology,SchoolofMedicine,JiangsuUniversity,Zhenjiang212013,China)
(2.DepartmentofRadiationOncology,AffiliatedPeople’sHospital,JiangsuUniversity,Zhenjiang212013,China)
关键词:
胰腺癌汉防己甲素Egr-1细胞自噬细胞凋亡
Keywords:
pancreaticcancertetrandrineEgr-1autophagycellapoptosis
分类号:
R730.5
文献标志码:
A
摘要:
本实验将胰腺癌细胞PaTu8988分别转染无关干扰对照组(siRNA-Scramble)和干扰即刻早期基因Egr-1组(siRNA-Egr-1),再用不同浓度的汉防己甲素处理24h后,CCK-8法检测不同浓度的汉防己甲素对细胞活力的影响;Westernblot检测细胞自噬和凋亡相关蛋白表达水平的改变.结果表明:(1)低浓度的汉防己甲素能显著激活PaTu8988细胞自噬,但对增殖和凋亡无明显影响;(2)与对照组相比,转染了siRNA-Egr-1组自噬相关蛋白Beclin-1表达量显著下降,LC3II/LC3I比值下调;凋亡相关蛋白Bcl2/Bax的比值降低.上述结果表明,干扰即刻早期基因Egr-1的表达可以有效抑制低浓度汉防己甲素引起的胰腺癌细胞PaTu8988自噬,促进细胞凋亡.
Abstract:
HumanpancreaticcancercellsPaTu8988weretransfectedwithsiRNA-ScrambleandsiRNA-Egr-1for24hrespectively,thentreatedwithtetrandrineforanother24h.Treatedbydifferentconcentrationoftetrandrine,thecytotoxiceffectoftetrandrinewasexaminedbyCCK-8,andexpressionofautophagy-relatedproteinweredetectedbyWesternblot.Theexpressionofcellautophagy-andapoptosis-relatedproteinweredetectedbyWesternblot.Alloftheresultsindicatedthatcomparingwithcontrolgroup,siEgr-1significantlyattenuatestetrandrine-inducedautophagyandpromotestheapoptosisofPaTu8988cells.

参考文献/References:

[1]HeY,ZhengR,LiD,etal.PancreaticcancerincidenceandmortalitypatternsinChina,2011[J].ChineseJournalofCancerResearch,2015,27(1):29.
[2]TangSC,ChenYC.Noveltherapeutictargetsforpancreaticcancer[J].WorldJournalofGastroenterology:WJG,2014,20(31):10825.
[3]GongK,ChenC,ZhanY,etal.Autophagy-relatedgene7(ATG7)andreactiveoxygenspecies/extracellularsignal-regulatedkinaseregulatetetrandrine-inducedautophagyinhumanhepatocellularcarcinoma[J].JBiolChem,2012,287(42):35576-35588.
[4]MeiL,ChenY,WangZ,etal.Synergisticanti-tumoureffectsoftetrandrineandchloroquinecombinationtherapyinhumancancer:apotentialantagonisticroleforp21[J].BrJPharmacol,2015,172(9):2232-2245.
[5]BaekKH,ParkJ,ShinI.Autophagy-regulatingsmallmoleculesandtheirtherapeuticapplications[J].ChemSocRev,2012,41(8):3245-3263.
[6]LiY,LuoP,WangJ,etal.AutophagyblockadesensitizestheanticanceractivityofCA-4viaJNK-Bcl-2pathway[J].ToxicologyandAppliedPharmacology,2014,274(2):319-327.
[7]HanMW,LeeJC,ChoiJY,etal.AutophagyinhibitioncanovercomeradioresistanceinbreastcancercellsthroughsuppressionofTAK1activation[J].AnticancerResearch,2014,34(3):1449-1455.
[8]LorinS,Hama?A,MehrpourM,etal.Autophagyregulationanditsroleincancer[C]//SeminarsinCancerBiology.Manhattan,NewYork:AcademicPress,2013.
[9]SteevesMA,DorseyFC,ClevelandJL.Targetingtheautophagypathwayforcancerchemoprevention[J].CurrentOpinioninCellBiology,2010,22(2):218-225.
[10]CarewJS,NawrockiST,ClevelandJL.Modulatingautophagyfortherapeuticbenefit[J].Autophagy,2007,3(5):464-467.
[11]RubinszteinDC,GestwickiJE,MurphyLO,etal.Potentialtherapeuticapplicationsofautophagy[J].NatureReviewsDrugDiscovery,2007,6(4):304-312.
[12]LiD,XieK,WolffR,etal.Pancreaticcancer[J].TheLancet,2004,363(9414):1049-1057.
[13]JemalA,SiegelR,XuJ,etal.Cancerstatistics,2010[J].CA:ACancerJournalforClinicians,2010,60(5):277-300.
[14]YangS,WangX,ContinoG,etal.Pancreaticcancersrequireautophagyfortumorgrowth[J].Genes&Development,2011,25(7):717-729.
[15]KangR,TangD,SchapiroNE,etal.Thereceptorforadvancedglycationendproducts(RAGE)sustainsautophagyandlimitsapoptosis,promotingpancreatictumorcellsurvival[J].CellDeath&Differentiation,2010,17(4):666-676.
[16]FujiiS,MitsunagaS,YamazakiM,etal.Autophagyisactivatedinpancreaticcancercellsandcorrelateswithpoorpatientoutcome[J].CancerScience,2008,99(9):1813-1819.
[17]ZhuR,LiuT,TanZ,etal.Tetrandrineinducesapoptosisingallbladdercarcinomainvitro[J].InternationalJournalofClinicalPharmacologyandTherapeutics,2014,52(10):900-905.
[18]ChenLM,LiangYJ,ZhangX,etal.ReversalofP-gp-mediatedmultidrugresistancebyBromotetrandrineinvivoisassociatedwithenhancedaccumulationofchemotherapeuticaldrugintumortissue[J].AnticancerRes,2009,29(11):4597-4604.
[19]LiX,SuB,LiuR,etal.TetrandrineinducesapoptosisandtriggersCaspasecascadeinhumanbladdercancercells[J].JSurgRes,2011,166(1):e45-e51.
[20]LiuC,GongK,MaoX,etal.TetrandrineinducesapoptosisbyactivatingreactiveoxygenspeciesandrepressingAktactivityinhumanhepatocellularcarcinoma[J].InternationalJournalofCancer,2011,129(6):1519-1531.
[21]WangH,LiuT,LiL,etal.Tetrandrineisapotentcellautophagyagonistviaactivatedintracellularreactiveoxygenspecies[J].Cell&Bioscience,2015,5(1):4-12.
[22]LeeBS,KangS,KimKA,etal.MetdegradationbySAIT301,aMetmonoclonalantibody,reducestheinvasionandmigrationofnasopharyngealcancercellsviainhibitionofEGR-1expression[J].CellDeath&Disease,2014,5(4):e1159.
[23]SunS,NingX,ZhaiY,etal.Egr-1mediateschronichypoxia-inducedrenalinterstitialfibrosisviathePKC/ERKpathway[J].AmericanJournalofNephrology,2014,39(5):436-448.

备注/Memo

备注/Memo:
收稿日期:2014-10-05.
基金项目:国家自然科学基金(31100964)、江苏省博士后基金(1402102C)、江苏大学高级人才科研启动基金(10JDG045).
通讯联系人:吴朝阳,博士,主任医师,研究方向:肿瘤耐药时间.E-mail:wuchaoyang9@163.com
更新日期/Last Update: 2015-09-30