表没食子儿茶素没食子酸酯(egcg)对鼻咽癌cne2细胞端粒酶活性影响。-肿瘤放疗学专业论文 word格式.docxVIP

白表达的影响。【结果】1.EGCG对鼻咽癌CNE2细胞株的增殖具有明显抑制作用，且呈现时间及药物浓度依赖性。2. EGCG具有阻滞鼻咽癌CNE2细胞周期进展作用，使G0/G1期比例升高（P0.001），S期比例下降（P0.002）。低浓度组（100 ug/mL）细胞周期阻滞呈时间依赖性，随着浓度增大及作用时间廷长细胞周期阻滞时间依赖性不明显，但细胞凋亡率升高。3. EGCG具有促鼻咽癌CNE2细胞凋亡作用，随着作用时间廷长其凋亡率升高（P0.001），呈时间依赖性。4.EGCG具有下调鼻咽癌CNE2细胞株hTERTmRNA（P0.001）及其蛋白的表达，且两者成正相关性。EGCG具有下调鼻咽癌CNE2细胞株c-Myc蛋白的表达，且与hTERTmRNA及其蛋白的表达呈正相关性。【结论】EGCG对鼻咽癌CNE2细胞株具有抑制增殖，促进凋亡作用，其可能原因是通过下调鼻咽癌CNE2细胞株C-Myc蛋白的表达从而抑制了hTERTmRNA的转录及hTERT 蛋白翻译，造成端粒酶的活性下降。【关键词】端粒酶端粒酶逆转录蛋白表没食子儿茶素没食子酸酯鼻咽癌CNE2细胞[Background]ABSTRACTNasopharyngeal carcinoma(NPC) is a common malignant tumor of the head and neck,anditsmainclinicaltreatmentareradiotherapyandchemotherapy.Althoughwiththe development of intensity-modulated radiotherapytechniques，the curerate ofNPC hasbeenincreasedanditssideeffectshasbeenreduced,the5-yearoverallsurvivalrateof patientswithadvancedstageofthecancerisstillnotideal,andtheside-effectsafter radiotherapystillcannotbeneglected,andthemultidrugrisistance(MDR)after chemotherapyisstillunavoidable.It’simperativetofindanewkindofanticancerdrugs withhighefficiencyandfewersideeffectsEpigallocatechin-3-gallate(EGCG),themain componentofgreenteapolyphenols,isakindofnaturalcompoundwithhighefficiencyin anti-cancerandlowtoxicityinnormalcells.Therefore,itisnotonlysignificanttostudy thepharmacologicalmechanismofEGCGagainstNPC,butalsopromisingforclinical practice.AlotofstudieshaveconfirmedthatEGCGcaninhibittumorcellsproliferationand promoteapoptosisoftumorcells[1-3].Butitsmechanismstillunclear.TheTelomeraseis aDNApolymerasewithreversetranscriptaseactivity,itispivotalforcellgrowth.Mostof thehumansomaticcellsdonn’torhavelowtelomeraseactivity,theirdivisiontimesis limited,andthecellsgotowardsagingandapoptosisfinally.Asforasmallnumberof humansomaticcells,somegermlinecellsandthemajorityoftumorcells(approximately 90%)thetelomereswillnotbeshortenedduetoreplication,andcellsgoto immortalization.Telomerasecontainsareversetranscriptaseprotein(humanoftelomerase reversetranscriptaseactivityofthereversetranscriptase,