简介：Objective:Humanpancreaticcancerisoneofthemostcommonclinicalmalignancies.Theeffectofcomprehensivetreatmentbasedonsurgeryisgeneral.Theeffectsofchemotherapywerenotobviousmainlybecauseoflackoftargetingandchemoresistanceinpancreaticcancer.Thisstudyaimedtoinvestigatetheeffectsoffolatereceptor(FR)-mediatedgemcitabineFA-Chi-Gemnanoparticleswithacore-shellstructurebyelectrostaticsprayonpancreaticcancer.Methods:Inthisstudy,thelevelsofexpressionofFRinsixhumanpancreaticcancercelllineswerestudiedbyimmunohistochemicalanalysis.Theuptakerateofisothiocyanate-labeledFA-ChinanoparticlesinFRhighexpressioncelllineCOLO357wasassessedbyfluorescencemicroscopeandtheinhibitionrateofFAChi-GemnanoparticlesonCOLO357cellswasevaluatedbyMTTassay.Moreover,thebiodistributionofPEG-FA-ICGDER02-Chiintheorthotopicpancreatictumormodelwasobservedusingnear-infraredimagingandthehumanpancreaticcancerorthotopicxenograftsweretreatedwithdifferentnanoparticlesandnormalsalinecontrol.Results:TheexpressionofFRinCOLO357wasthehighestamongthesixpancreaticcancercelllines.TheFRmainlydistributedoncellmembraneandfewerinthecytoplasminpancreaticcancer.Moreover,theabsorptionrateoftheFA-Chi-GemnanoparticleswasmorethantheChinanoparticleswithoutFAmodified.TheproliferationofCOLO357wassignificantlyinhibitedbyFA-Chi-Gemnanoparticles.ThePEG-FAICGDER02-Chinanoparticleswereenrichedintumortissueinhumanpancreaticcancerxenografts,whilenon-targetednanoparticlesweremainlyinnormallivertissue.PEG-FA-Gem-Chisignificantlyinhibitedthegrowthofhumanpancreaticcancerxenografts(PEG-FA-Gem-Chivs.Gem,t=22.950,P=0.000).Conclusions:PEG-FA-FITC-ChinanoparticlesmightbeaneffectivetargeteddrugfortreatinghumanFR-positivepancreaticcancer.

简介：Glioblastoma(GBM)isoneofthemostlethalhumancancers.GenomicanalysesdefinethemoleculararchitectureofGBMandhighlightacentralfunctionformechanistictargetofrapamycin(mTOR)signaling.mTORkinaseexistsintwomultiproteincomplexes,namely,mTORC1andmTORC2.Thesecomplexesdifferintermsoffunction,regulationandrapamycinsensitivity.mTORC1iswellestablishedasacancerdrugtarget,whereasthefunctionsofmTORC2incancer,includingGBM,remainspoorlyunderstood.ThisstudyreviewstherecentfindingsthatdemonstrateacentralfunctionofmTORC2inregulatingtumorgrowth,metabolicreprogramming,andtargetedtherapyresistanceinGBM,whichmakesmTORC2asacriticalGBMdrugtarget.