Overexpressed Galectin-3 in Pancreatic Cancer Induces Cell Proliferation and Invasion by Binding Ras and Activating Ras Signaling 英文参考文献.docVIP

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Overexpressed Galectin-3 in Pancreatic Cancer Induces Cell Proliferation and Invasion by Binding Ras and Activating Ras Signaling 英文参考文献.doc

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Overexpressed Galectin-3 in Pancreatic Cancer Induces Cell Proliferation and Invasion by Binding Ras and Activating Ras Signaling 英文参考文献

OverexpressedGalectin-3inPancreaticCancerInduces CellProliferationandInvasionbyBindingRasand ActivatingRasSignaling ShumeiSong1*,BaoanJi2,VijayaRamachandran2,HuaminWang3,MargareteHafley1,CraigLogsdon2, RobertS.Bresalier1 1DepartmentofGastroenterology,Hepatology,andNutrition,UniversityofTexasMDAndersonCancerCenter,Houston,Texas,UnitedStatesofAmerica,2Department of Cancer Biology, University of Texas MD Anderson Cancer Center, Houston, Texas, United States of America, 3Department of Pathology, University of Texas MD AndersonCancerCenter,Houston,Texas,UnitedStatesofAmerica Abstract Pancreaticcancer(PDAC)isalethaldiseasewithafive-yearsurvivalof3–5%.MutationsinK-Rasarefoundinnearlyallcases, butK-RasmutationsalonearenotsufficientforthedevelopmentofPDAC.AdditionalfactorscontributetoactivationofRas signaling and lead to tumor formation. Galectin-3 (Gal-3), a multifunctional b-galactoside-binding protein, is highly expressed in PDAC. We therefore investigated the functional role of Gal-3 in pancreatic cancer progression and its relationship to Ras signaling. Expression of Gal-3 was determined by immunohistochemistry, Q-PCR and immunoblot. FunctionalstudieswereperformedusingpancreaticcelllinesgeneticallyengineeredtoexpresshighorlowlevelsofGal-3. RasactivitywasexaminedbyRafpull-downassays.Co-immunoprecipitationandimmunofluorescencewereusedtoassess protein-proteininteractions.Inthisstudy,wedemonstratethatGal-3washighlyup-regulatedinhumantumorsandina mutantK-RasmousemodelofPDAC.Down-regulationofGal-3bylentivirusshRNAdecreasedPDACcellproliferationand invasioninvitroandreducedtumorvolumeandsizeinanorthotopicmousemodel.Gal-3boundRasandmaintainedRas activity;down-regulationofGal-3decreasedRasactivityaswellasRasdown-streamsignalingincludingphosphorylationof ERKandAKTandRalAactivity.TransfectionofGal-3cDNAintoPDACcellswithlow-levelGal-3augmentedRasactivityand itsdown-streamsignaling.TheseresultssuggestthatGal-3contributestopancreaticcancerprogression,inpart,bybinding Rasandactivatin