異甘草素體外抗腫瘤活性及作用機制研究的綜述報告

異甘草素體外抗腫瘤活性及作用機制研究的綜述報告異甘草素是從甘草根部提取得到的一種天然化合物，具有多種生物活性，如抗氧化、抗炎、抗微生物等。近年來，其抗腫瘤活性備受關注。本文將從異甘草素的體外抗腫瘤活性和作用機制兩個方面進行綜述。一、異甘草素的體外抗腫瘤活性1.抑制細胞增殖和誘導細胞凋亡Studieshaveshownthatisoliquiritigeninexhibitsstrongantiproliferativeandproapoptoticeffectsinvariouscancercelllines.Forexample,isoliquiritigenincaninhibittheproliferationofbreastcancercellsinadose-andtime-dependentmannerandinducecellcyclearrestintheG2/Mphase.Moreover,isoliquiritigenincaninduceapoptosisinbreastcancercellsviatheactivationofcaspase-3andtheBax/Bcl-2pathway.Inaddition,isoliquiritigeninhasbeenreportedtoexhibitpotentantiproliferativeeffectsinhumanlungcancercells,colonadenocarcinomacells,gastriccancercells,andprostatecancercells.Theunderlyingmechanismofitsantiproliferativeactivityismainlyattributedtotheinductionofapoptosis,cellcyclearrest,andinhibitionofthePI3K/AktandNF-κBsignalingpathways.2.抑制腫瘤細胞侵襲和轉(zhuǎn)移Metastasisisamajorcauseofcancer-relatedmorbidityandmortality.Studieshavefoundthatisoliquiritigenincaninhibittheinvasionandmetastasisofvariouscancercells.Forexample,isoliquiritigenincanreducethemigrationandinvasionofbreastcancercellsthroughthedownregulationofMMP-9expressionandtheinhibitionofthePI3K/AktandERKsignalingpathways.Similarly,isoliquiritigenincanalsoinhibitthemigrationandinvasionofhumanlungcancercellsandgastriccancercellsbydownregulatingthelevelsofMMP-2andMMP-9.3.抑制腫瘤血管生成Angiogenesis,theformationofnewbloodvessels,playsacrucialroleintumorgrowthandmetastasis.Studieshaveshownthatisoliquiritigenincaninhibitangiogenesisbytargetingvarioussignalingpathways.Forinstance,isoliquiritigenincandownregulatetheexpressionofVEGF,akeyfactorinangiogenesis,inbreastcancercellsandhumanumbilicalveinendothelialcells.Moreover,isoliquiritigenincaninhibittheactivationoftheAktandERKsignalingpathways,whichareinvolvedintheregulationofangiogenesis.4.其他作用Inadditiontotheabove-mentionedantitumoreffects,isoliquiritigeninhasbeenreportedtoexertotheractivities,suchasmodulatingtheimmuneresponse,enhancingthesensitivityofcancercellstochemotherapydrugs,andinhibitingthestemnessofcancercells.二、異甘草素的作用機制1.抑制凋亡途徑Studieshaveshownthatisoliquiritigenincaninduceapoptosisincancercellsviamultiplepathways.Forexample,isoliquiritigenincanactivatecaspase-3andtheBax/Bcl-2pathway,whichareimportantregulatorsofapoptosis.Moreover,isoliquiritigenincaninhibittheNF-κBandPI3K/Aktsignalingpathways,whichareinvolvedincellproliferationandsurvival.2.抑制信號轉(zhuǎn)導通路ThePI3K/Aktsignalingpathwayplaysacriticalroleincellgrowthandsurvival,anditsdysregulationhasbeenimplicatedinthedevelopmentofmultiplecancers.StudieshavefoundthatisoliquiritigenincaninhibittheactivationofthePI3K/AktpathwaybydownregulatingtheexpressionofPI3K,Akt,andmTOR.Similarly,isoliquiritigenincaninhibittheactivationoftheERK1/2andJNKsignalingpathways,whichareinvolvedincellproliferationandmetastasis.3.調(diào)節(jié)轉(zhuǎn)錄因子和基因表達Isoliquiritigeninhasbeenshowntomodulatetheexpressionofvariousgenesandtranscriptionfactorsinvolvedincellgrowth,apoptosis,andmetastasis.Forinstance,isoliquiritigenincanupregulatetheexpressionofp53,atumorsuppressorgene,anddownregulatetheexpressionofcyclinD1,akeyregulatorofthecellcycle.Moreover,isoliquiritigenincanmodulatetheexpressionofVEGF,MMPs,andEMT-relatedgenes,whichareinvolvedinangiogenesis,invasion,andmetastasis.4.其他機制Inadditiontotheabove-mentionedmechanisms,isoliquiritigeninhasbeenreportedtoexertitsantitumoreffectsthroughmodulatingtheoxidativestress,autophagy,and