乳腺癌细胞中与舞茸DFraction诱导的恶性表型抑制相关的基因文档格式.docx

乳腺癌细胞中与舞茸DFraction诱导的恶性表型抑制相关的基因文档格式.docx

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【参考译文】

JournalofMedicinalFood16（7）2013,602-617

GenesRelatedtoSuppressionofMalignantPhenotypeInducedbyMitakeD-FractioninBreastCancerCells

乳腺癌细胞中与舞茸D-Fraction诱导的恶性表型抑制相关的基因

Abstract翻译参考

我们已经知道舞茸D-Fraction参与刺激免疫系统并激活那些能攻击癌症的细胞，如巨噬细胞、T细胞、NK细胞。

根据美国国家癌症协会宣布，舞茸中的多糖复合物表现出显著的抗癌活性。

尽管如此，舞茸抗癌的确切分子机制仍不清楚。

我们曾报道舞茸D-Fraction通过激活BAK1基因表达诱导乳腺癌细胞凋亡。

在目前的工作中，我们正在确认在乳腺癌细胞中由舞茸D-Fraction引起的抑制肿瘤现象，其机制中起主要作用的基因究竟是哪一个。

人类乳腺癌细胞MCF-7细胞分别用递增浓度的舞茸D-Fraction（36，91,183,367μg/ml）处理24小时。

分离所有的RNA，基因芯片杂交包括25000个人类基因。

利用基因芯片分析，我们发现，在这个依剂量的24小时实验中，舞茸D-Fraction改变了MCF-7乳腺癌细胞中4068个基因的表达（2420个增加，1648个减少）。

目前的数据显示，舞茸D-Fraction通过假定的分子机制抑制乳腺癌表型，即改变特定基因的表达（如：

IGFBP-7，ITGA2,ICAM3,SOD2,CAV-1,Cul-3,NRF2,CyclineE,ST7,andSPARC）,这与凋亡刺激、阻止细胞生长和增殖、细胞周期阻滞、阻止癌细胞转移、以及诱导多药物敏感性等有关。

所有这些结果表明舞茸D-fraction能作为乳腺癌化学预防和治疗的潜在新目标。

【论文原文】

JMedFood16（7）2013,602–617

GenesRelatedtoSuppressionofMalignantPhenotypeInducedbyMaitakeD-FractioninBreastCancerCells

ElianaNoeliaAlonso,ManuelaOrozco,AlvaroEloyNieto,andGabrielaAndreaBalogh

BiotechnologyLaboratory,ScienceandTechnologyCenter,CenterofRenewableNaturalResourcesoftheSemi-AridZone（CERZOS）,NationalScientificandTechnicalResearchCouncil（CONICET）,BahiaBlanca,BuenosAires,Argentina.

ABSTRACT 

ItisalreadyknownthattheMaitake（D-Fraction）mushroomisinvolvedinstimulatingtheimmunesystemandactivatingcertaincellsthatattackcancer,includingmacrophages,T-cells,andnaturalkillercells.AccordingtotheU.S.NationalCancerInstitute,polysaccharidecomplexespresentinMaitakemushroomsappeartohavesignificantanticanceractivity.However,theexactmolecularmechanismoftheMaitakeantitumoraleffectisstillunclear.Previously,wehavereportedthatMaitake（D-Fraction）inducesapoptosisinbreastcancercellsbyactivationofBCL2-antagonist/killer1（BAK1）geneexpression.Atthepresentwork,weareidentifyingwhichgenesareresponsibleforthesuppressionofthetumoralphenotypemechanisminducedbyMaitake（D-Fraction）inbreastcancercells.HumanbreastcancerMCF-7cellsweretreatedwithandwithoutincreasedconcentrationsofMaitakeD-Fraction（36,91,183,367lg/mL）for24h.TotalRNAwereisolatedandcDNAmicroarrayswerehybridizedcontaining25,000humangenes.EmployingthecDNAmicroarrayanalysis,wefoundthatMaitakeD-Fractionmodifiedtheexpressionof4068genes（2420wereupmodulatedand1648weredownmodulated）inMCF-7breastcancercellsinadose-dependentmannerduring24hoftreatment.ThepresentdatashowsthatMaitakeD-Fractionsuppressesthebreasttumoralphenotypethroughaputativemolecularmechanismmodifyingtheexpressionofcertaingenes（suchasIGFBP-7,ITGA2,ICAM3,SOD2,CAV-1,Cul-3,NRF2,CyclineE,ST7,andSPARC）thatareinvolvedinapoptosisstimulation,inhibitionofcellgrowthandproliferation,cellcyclearrest,blockingmigrationandmetastasisoftumoralcells,andinducingmultidrugsensitivity.Altogether,theseresultssuggestthatMaitakeD-Fractioncouldbeapotentialnewtargetforbreastcancerchemopreventionandtreatment.

KEYWORDS:

·

breastcancercells·

geneexpression·

MaitakeD-Fraction·

malignantphenotype 

microarrays

INTRODUCTION

NumerousstudieshaveconfirmedthatMaitakehasprominentbeneficialeffectsonimmunefunction.1-9Itpromotestheactionofnotonlymacrophages,butalsoavarietyofotherimmune-relatedcells,suchasnaturalkiller（NK）cellsandcytotoxicT-cellsthatcanattacktumorcells.Maitakealsoincreasestheimmune-relatedefficiencyofthesecellsbyincreasinginterleukin-1,interleukin-2,andlymphokines.1-9

ThespecificproteoglucanintheMaitakemushroomextractforfightingcancertumorsiscalledD-Fraction.MaitakeD-Fractionhasbeenreportedtoexertitsantitumoreffectintumor-bearingmicebyenhancingtheimmunesystemthroughactivationofmacrophages,Tcells,andNKcells.Theproteoglucanshowsanticarcinogenicactivity,preventsoncogenesis,andpreventsmetastasis.However,theexactmolecularmechanismsandgeneexpressionprofilesgeneratedbyMaitakeD-Fractionintheanticarcinogenesisprocessarestillunclear.Inourpreviouswork,wehavedemonstratedthatD-FractionofMaitakemushroomwasabletoeffectivelyinduceapoptosisinMCF-7breastcancercells.10Thesefindingswerecorroboratedbyareductionincellviabilityupontreatmentwithdifferentconcentrationsofthisfraction.SeveralgenespromotingapoptosiswereupregulatedasassessedbycDNAmicroarrayanalysis.WehavereportedthatD-FractionStandard