mir-21调控舌鳞癌细胞凋亡的实验研究

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1、中山大学博士学位论文miR．2l调控舌鳞癌细胞凋亡的实验研究However,whatisthebiologymechanismforgeneregulationandexpressionchangeintheprocessofTSCC?Althoughnocertainresult，non·codingRNAs，especiallymicroRNAs(miRNAs)，inspiretheresearchers．Itisknownthattumorigenesisreferstomultiplegenev

2、ariationandsinglegeneinterventioncannotinhabittumoranditsprogress．AsendogenousmiRNAcanregulateafeworhundredsgenes；besides，thosemiRNAsaremuchlessthanthecodinggenes，theyshouldbethestableandeffectiveanti—tumortargets．StudieshaveindicatedthatmiRNAsparticipat

3、einaseriallifeprocess，includinggrowth，hematopoiesis，organ—formation，apoptosis，cellproliferationandtumorigenesis．Theoncogeneoranti—oncogenemiRNAscorrelatewithcellproliferation，apoptosisanddifferentiation．Recently,highthroughputmicroarrayassayandquantitati

4、verealtimeRT-PCR(qRT-PCR)inresearchofcoloncancer,breastcancer,lungcancer，renalcancer，gastriccancer，lymphoma，leukemia,eta1．revealmiRNAsprofileofcancersandthechangesfromtheoriginallynormaltissues．Researchesindicatethattumors’malignancypositivelycorrelatedw

5、iththemiRNAchangeandinsomeadvancedcancer’certainmiRNAexpressionlevelsareevenlower．Inbreastcancer，miR一10b，let一7，miR一125bandmiR-145aredown-regulated，whilesomemiRNAsareup-regulated，likemiR一21andmiR一155．ThosealterationsofmiRNAsintumorsuggesttheeffectsofgener

6、egulation．ForheadandneckcancelparticularlytheTSCC，miRNAsandtheirfunctionsaleseldomstudied．WeemployedhighthroughputmicroarrayassaytoscreendifferentialexpressionofendogenousmiRNAsinTSCCtissuesofdifferentclinicalstagesandnormaltissue．ThenwefocusedonthemiR一2

7、1whichhassignificantlyhighexpressioninbothearlyandadvancedTSCC．Wecollected50independentsamplesofTSCCpatientsofdifferentclinicalstagesandusedqRT-PCRtotestifythedifferentialexpressionofmiR一21．Meanwhile，weusedimmunohistochemistrytechnologytodeterminetheexpr

8、essionoftropomyosin—I(TPM—1)，thetargetofmiR一21，inthesame50samples．AndwedetectedcellapoptosisbyTunelapoptosisdetectionkit．Combinedwithpatients’clinicdata，weanalyzedtherelationshipamongthoseindexes．Basedonthoseresults—VIII—中