HBx对SOCS-1CpG岛甲基化及其表达的影响-豆柴文库

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HBx对SOCS-1CpG岛甲基化及其表达的影响
Title:TheInfluenceofHBxonSOCS-1CpGIslandMethylationandItsExpression
Abstract:
HepatitisBvirus(HBV)infectionisamajorglobalhealthconcern,andchronicinfectionoftenleadstothedevelopmentofliverdiseases,includinghepatocellularcarcinoma(HCC).TheHBV-encodedXprotein(HBx)hasbeenwidelyreportedtoplayacrucialroleinHBVpathogenesis.ThispaperaimstoexploretheinfluenceofHBxonthemethylationstatusofthesuppressorofcytokinesignaling1(SOCS-1)CpGislandanditssubsequentimpactongeneexpression.
Introduction:
HepatitisBvirus(HBV)istheleadingcauseofliverdiseases,includingchronichepatitis,liverfibrosis,cirrhosis,andhepatocellularcarcinoma(HCC).TheHBVXprotein(HBx)isamultifunctionalviralproteinthathasbeenimplicatedinvariousprocesses,includingviralreplication,immuneevasion,andcellulartransformation.Thesuppressorofcytokinesignaling1(SOCS-1)isanegativeregulatoroftheJanuskinase/SignalTransducerandActivatorofTranscription(JAK/STAT)pathwayandplaysacriticalroleinmodulatingtheimmuneresponse.
Methods:
ToinvestigatetheinfluenceofHBxonSOCS-1CpGislandmethylationanditsexpression,bothinvitroandinvivoexperimentswereconducted.HepG2cellsweretransfectedwithanHBxexpressionplasmid,andthemethylationstatusandgeneexpressionofSOCS-1wereanalyzed.Inaddition,livertissuesfromHBV-infectedpatientsandHBxtransgenicmicewereexaminedforSOCS-1methylationlevelsandexpression.
Results:
OurresultsshowedthatHBxexpressionledtoasignificantincreaseinthemethylationstatusoftheSOCS-1CpGislandinHepG2cells.ThisincreaseinmethylationwasaccompaniedbyadecreaseinSOCS-1geneexpression.Consistentwiththesefindings,livertissuesfromHBV-infectedpatientsandHBxtransgenicmicedemonstratedhigherlevelsofSOCS-1CpGislandmethylationandreducedSOCS-1expressioncomparedtocontrols.
Discussion:
TheHBx-mediatedincreaseinSOCS-1CpGislandmethylationsuggestsapotentialmechanismbywhichHBVmanipulateshostgeneexpressiontopromoteviralreplicationandpathogenesis.SOCS-1downregulationhasbeenassociatedwithincreasedcellproliferationandsurvival,enhancedinvasionandmig