Rgs2 Mediates Pro-Angiogenic Function of Myeloid Derived Suppressor Cells in the Tumor Microenvironment via Upregulation of MCP-1 英文参考文献.docVIP

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Rgs2 Mediates Pro-Angiogenic Function of Myeloid Derived Suppressor Cells in the Tumor Microenvironment via Upregulation of MCP-1 英文参考文献.doc

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Rgs2 Mediates Pro-Angiogenic Function of Myeloid Derived Suppressor Cells in the Tumor Microenvironment via Upregulation of MCP-1 英文参考文献

Rgs2MediatesPro-AngiogenicFunctionofMyeloid DerivedSuppressorCellsintheTumor MicroenvironmentviaUpregulationofMCP-1 KimberlyC.Boelte1,LauraE.Gordy2,SebastianJoyce2,MaryAnnThompson3,LiYang4,P.CharlesLin4* 1DepartmentofCancerBiology,VanderbiltUniversityMedicalCenter,Nashville,Tennessee,UnitedStatesofAmerica,2DepartmentofMicrobiologyandImmunology, Vanderbilt University Medical Center, Nashville, Tennessee, United States of America, 3Department of Pathology, Vanderbilt University Medical Center, Nashville, Tennessee,UnitedStatesofAmerica,4CenterforCancerResearch,NationalInstitutesofHealth,Bethesda,Maryland,UnitedStatesofAmerica Abstract Background: Tumor growth is intimately linked with stromal interactions. Myeloid derived suppressor cells (MDSCs) are dramaticallyelevatedincancerpatientsandtumorbearingmice.MDSCsmodulatethetumormicroenvironmentthrough attenuatinghostimmuneresponseandincreasingvascularization. Methodology/PrincipalFindings:Insearchingformolecularmediatorsresponsibleforpro-tumorfunctions,wefoundthat regulator of G protein signaling-2 (Rgs2) is highly increased in tumor-derived MDSCs compared to control MDSCs. We further demonstrate that hypoxia, a common feature associated with solid tumors, upregulates the gene expression. GeneticdeletionofRgs2inmiceresultedinasignificantretardationoftumorgrowth,andthetumorsexhibitdecreased vascular density and increased cell death. Interestingly, deletion of Rgs2 in MDSCs completely abolished their tumor promotingfunction,suggestingthatRgs2signalinginMDSCsisresponsibleforthetumorpromotingfunction.Cytokine arrayprofilingidentifiedthatRgs22/2tumorMDSCsproducelessMCP-1,leadingtodecreasedangiogenesis,whichcould berestoredwithadditionofrecombinantMCP-1. Conclusion: Our data reveal Rgs2 as a critical regulator of the pro-angiogenic function of MDSCs in the tumor microenvironment,throughregulatingMCP-1production. Citation:BoelteKC,GordyLE,JoyceS,ThompsonMA,YangL,etal.(2011)Rgs2MediatesPro-AngiogenicFunctionofMyeloidDerivedSu