面向生物学对象的离子治癌模式的初步研究的中期报告.docxVIP

面向生物学对象的离子治癌模式的初步研究的中期报告

Introduction

Cancerisacrucialpublichealthissueworldwide,anditremainsaleadingcauseofdeath.Despitemanytreatmentoptionsavailable,suchaschemotherapyandradiationtherapy,theeffectivenessofthesetherapiesislimitedowingtotheirnonselectivecytotoxicityagainstbothcancerousandnormalcells.Recently,ionchannelsandtransportershavebeenidentifiedasattractivetargetsandarerapidlyemergingasnoveltherapeuticcandidatestotreatvariouscancers.Inthisstudy,weaimtoinvestigatethepotentialofionchannelandtransporterinhibitorstotargetspecificsignalingpathwaysinbreastcancercells.

Methods

WeusedtheMCF7breastcancercelllineforourstudy.Toevaluatetheeffectofionchannelandtransporterinhibitorsonbreastcancercellproliferation,weconductedcellviabilityassaysusingtheMTTmethod.WemeasuredtheintracellularcalciumlevelinMCF7cellsusingtheFluo-4NWCalciumAssayKit.Furthermore,weusedwesternblotanalysistoevaluatetheeffectofionchannelandtransporterinhibitorsontheproteinexpressionlevelsofkeysignalingmoleculesinMCF7cells.

Results

Ourresultsindicatethatinhibitionofthevoltage-gatedpotassiumchannelKV1.3usingthespecificinhibitorcorreolidesignificantlyreducedbreastcancercellproliferation.Moreover,theintracellularcalciumlevelwassignificantlydecreasedupontreatmentwithcorreolide,indicatingtheinvolvementofKV1.3channelsincalciumsignalingpathways.Additionally,westernblotanalysisdemonstratedthatcorreolidesignificantlyreducedtheexpressionlevelsofkeyproteins,suchasERK1/2,phospho-ERK1/2,andcyclinA,indicatingtheinhibitoryeffectofcorreolideonthesesignalingpathways.

Discussion

OurfindingssuggestthatKV1.3channelsplayacrucialroleinbreastcancercellproliferationandtheregulationofsignalingpathwaysinvolvedinbreastcancer.Moreover,ourresultssupportthepotentia