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1、MedOncol(2015)32:254DOI10.1007/s12032-015-0696-6ORIGINALPAPERThehumanchemokinereceptorCCRL2suppresseschemotaxisandinvasionbyblockingCCL2-inducedphosphorylationofp38MAPKinhumanbreastcancercells1,31,31,31,31,3Lei-PingWang•JunCao•JianZhang•Bi-YunWang•Xi-ChunHu•2,31
2、,32,3Zhi-MinShao•Zhong-HuaWang•Zhou-LuoOuReceived:20June2015/Accepted:6October2015ÓSpringerScience+BusinessMediaNewYork2015AbstractThehumanchemokinereceptorCCRL2isainvitroandinvivo.OurresultssuggestthatCCRL2func-memberoftheatypicalchemokinereceptorfamily.CCRL2ti
3、onsasatumorsuppressorinhumanbreastcancercells.isunabletocouplewithG-proteinsandfailstoinduceclassicalchemokinesignalingforthehighlyconservedKeywordsBreastcancerCCRL2CCL2ChemotaxisDRYLAIVmotifessentialforsignalinghasbeenchangedInvasionp38MAPKtoQRYLVFL.Weinve
4、stigatedwhetherCCRL2isinvolvedinthechemotaxis,invasion,andproliferationofhumanbreastcancercells.Firstly,expressionofCCRL2wasIntroductiondeterminedinsixbreastcancercelllinesbyreal-timeRT-PCRandWesternblot.Then,weestablishedstablecellBreastcanceristhemostcommonlyd
5、iagnosedcancerinlinesoverexpressingCCRL2toexplorethefunctionofwomen[1],withmetastasisbeingthemajorcauseofdeathinCCRL2inchemotaxisandinvasionbytranswellassays,andbreastcancerpatients[2].Althoughthedetailedmechanismthesignalingdownstreamwasfurtherinvestigated.Theo
6、ftumormetastasisremainsunclear,manymoleculeshaveeffectofCCRL2onproliferationwasdetectedbycolonybeenidentifiedtopromotecancermetastasis[3,4].Che-formationassaysandtumorxenograftstudy.WefoundthatmokinereceptorsaretypicalG-protein-coupledreceptorsstableoverexpressio
7、nofCCRL2inMDA-MB-231andBT-(GPCRs)thatbindchemokineligandsandtriggerintracel-549cellsattenuatedthechemotaxisandinvasionstimulatedlularsignalingcascades.ChemokinereceptorsareknowntobyitsligandCCL2.CCRL2inhibitsp38MAPK(p38)beinvolvedininflammatoryresponses,angiogene
8、sis,aswellphosphorylationandup-regulatestheexpressionofE-cad-astumorgrowthandmetastasis[5,6].Atypicalchemokineherin.Thiseffectwaseliminatedbytheinhibitorofp38receptor
