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mir-630抑制胃癌细胞侵袭迁移和EMT机制的研究.docx

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mir-630抑制胃癌细胞侵袭迁移和EMT机制的研究 Title:TheInhibitionofGastricCancerCellInvasion,Migration,andEMTMechanismsbymiR-630:AStudy Abstract: Gastriccancer(GC)isahighlyprevalentandaggressivemalignancyworldwide.Thedevelopmentoftherapeuticstrategiestargetingspecificmolecularmechanismshasshownpromise.MicroRNAs(miRNAs)aresmallnon-codingRNAsinvolvedintheregulationofgeneexpressionandhaveemergedaspotentialtherapeutictargetsinseveralmalignancies,includingGC.ThisstudyaimstoinvestigatetheroleofmiR-630intheinhibitionofGCcellinvasion,migration,andepithelial-mesenchymaltransition(EMT)mechanisms. Introduction: Gastriccancerisamajorhealthconcernwithlimitedtreatmentoptionsandhighmortalityrates.UnderstandingtheunderlyingmolecularmechanismsinvolvedinGCprogressioncouldpotentiallyleadtothedevelopmentofnoveltherapeuticstrategies.EmergingevidencesuggeststhatdysregulationofmiRNAsplaysacrucialroleinGCprogression,withmiR-630beingimplicatedinvariousmalignancies.However,thespecificroleandmolecularmechanismsofmiR-630inGCremainlargelyunexplored. Methods: Inthisstudy,weutilizedGCcelllines(e.g.,MKN-45andAGS)toinvestigatethefunctionalroleofmiR-630inGC.Weemployedvarioustechniques,includingcellviabilityandproliferationassays,woundhealingassay,transwellinvasionassays,andWesternblotanalysis,toassesstheeffectsofmiR-630onGCcellinvasion,migration,andEMTmarkers.TheexpressionlevelsofkeygenesinvolvedintheEMTprocessweredeterminedbyquantitativereal-timepolymerasechainreaction(qRT-PCR). Results: OurfindingsdemonstratethatmiR-630issignificantlydownregulatedinGCcelllinescomparedtonormalgastricepithelialcells.OverexpressionofmiR-630inhibitedGCcellproliferation,migration,andinvasion.Moreover,miR-630suppressedtheexpressionofEMTmarkers,includingN-cadherin,Vimentin,Snail,andTwist.Conversely,upregulationofmiR-630resultedinincreasedexpressionofE-cadherin,akeyepithelialmarker. Discussion: OurstudysuggeststhatmiR-630actsasatumorsuppressorinGCbyinhibitingcellinvasion,migration,andtheEMTprocess.ItexertsitsinhibitoryeffectsbytargetingEMT-