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1、newsAndviewsCancerstemcells:natureversusnurtureHasanKorkayaandMaxS.Wichaalthoughallcellswithinacoloncancermayharbouradenomatouspolyposiscoli(aPC)orβ-cateninmutations,activationofwntsignallingislimitedtoasubpopulationofcellsthatdisplaycancerstemcellproperties.Thisactivationrequiresaco-stimulatorysign
2、almediatedbyhepatocytegrowthfactor,whichisproducedbytumour-associatedmyofibroblasts.Thecancerstemcellhypothesispositsthatthatstromal-derivedHGFactivatesthec-MetcellsonWntsignalling,thesecellsmayalsoaffecttumoursareorganizedinacellularhierarchyreceptorinthetumourcells,whichleadstoAktCSCpopulationsthr
3、oughmodulationofNotch7maintainedbyasubpopulationofcellsdisplay-activation,phosphorylationanddegradationofandHedgehog8pathways,whichregulatestemingstemcellproperties.ThesepropertiesincludeGSK-3β,aswellasphosphorylationofβ-catenincellself-renewalanddifferentiation.Inaddition,self-renewal(whichdrivestu
4、mourigenesis),andonserine552,therebyfacilitatingitsnuclearinflammatorycytokines,suchasinterleukin-6differentiation(whichgeneratesthetumourbulktranslocation.Inthenucleus,β-cateninactivates(IL-6;ref.9)andinterleukin-8(IL-8;ref.10)pro-andcontributestocellularheterogeneity).Theanumberoftranscriptionfact
5、orsincludingTCF/ducedbycellsinthetumourmicroenvironment,WntsignallingpathwayhasacrucialroleintheLEF(Fig.1).TherequirementforAktactivationmayregulateCSCself-renewalandsurvival.regulationofstemcellself-renewalinmanytis-toprovideaco-stimulatorysignalforWntsignal-InhibitorsofCXCR1,areceptorforIL-8,inhib
6、itsuesincludingthegut,andmutationsthatactivatelinghasalsorecentlybeenreportedtobeimpor-self-renewalandinduceapoptosisinbreastcan-thispathwayarepresentinthevastmajorityoftantforregulationofnormalandmalignantstemcerxenograftCSCs11.Theobservationthatcellscoloncancers1.However,ifWntactivationdrivescells
7、inthebreast3andotherorgans,suggestingthatdonotdisplayWntactivationfailedtoformstemcellself-renewalandifallofthecellswithinamoregeneralfunctionforthisco-stimulatorytumoursinxenograftsunlessmyofibroblas
