简介：Objective:Theaimofthepresentstudywastoanalyzetheprognosticfactorsinpatientswithhepatoblastoma(HB)inoursinglecenterandtoevaluateperiostin(POSTN)expressioninHBanditsassociationwithclinicopathologicalvariables.Inaddition,theunderlyingmechanismofhowPOSTNpromotesHBprogressionwasdiscussed.Methods:POSTNexpressionwasinvestigatedinHBtumorsbyimmunohistochemistry(IHC),immunofluorescence(IF)andWesternblot(WB).TheassociationamongPOSTNexpression,clinicopathologicalfeaturesandoverallsurvival(OS)wasalsoevaluated.ThemigrationandadhesionabilityofHBcellsweremeasuredusingchemotaxisandcell-matrixadhesionassays,respectively.Epithelial-mesenchymaltransition(EMT)-associatedmarkersandactivationoftheERKpathwayweredetectedbyWB.Results:HBpatientshadpoorprognosiswhichdisplayedlymphnodemetastasis,vascularinvasion,POSTNandvimentinexpression.POSTNexpressionwasalsoassociatedwithlymphnodemetastasis.Furthermore,overexpressedPOSTNpromotedmigrationandtheadhesiveabilityofHBcellsinvitro.Inaddition,wedemonstratedthatPOSTNactivatedtheMAPK/ERKpathway,upregulatedtheexpressionofSnailanddecreasedtheexpressionofOVOL2.Finally,POSTNpromotedtheexpressionofEMT-associatedmarkers.Conclusions:POSTNmightmodulateEMTviatheERKsignalingpathway,therebypromotingcellularmigrationandinvasion.OurstudyalsosuggeststhatPOSTNmayserveasatherapeuticbiomarkerinHBpatients.

简介：Objective:TodeterminewhetherInterferon-alpha-2b(IFN-α2b)canmodulatetheautophagicresponseinhepatocellularcarcinomacells.Methods:HepatocellularcarcinomacellsweretreatedwithIFN-α2b.Autophagywasassessedbyacridineorangestaining,GFP-LC3dottedassay,transmissionelectronmicroscopyandimmunoblotting.Results:AcridineorangestainingshowedthatIFN-α2btriggeredtheaccumulationofacidicvesicularandautolysosomesinHepG2cells.TheacridineorangeHepG2cellratioswere(4.3±1.0)%,(6.9±1.4)%,and(13.1±2.3)%,respectively,aftertreatmentwith100,1,000,and10,000IU/mLIFN-α2bfor48h.AmarkedlypunctatepatternwasobservedinHepG2cellstreatedwith10,000IU/mLIFN-α2bfor48h,butonlydiffuseandweaklyfluorescentGFP-LC3punctawasobservedincontrolcells.HepG2cellstreatedwith10,000IU/mLIFN-α2bfor48hdevelopedautophagosome-likecharacteristics,includingsingle-ordouble-membranevacuolescontainingintactanddegradedcellulardebris.TheBeclin1andLC3-IIproteinexpressionwasup-regulatedbyIFN-α2btreatment.Conclusion:Autophagycanbeinducedinadose-dependentmannerbytreatmentwithIFN-α2binHepG2cells,andtheBeclin1signalingpathwaywasstimulatedbyIFN-α2b.

简介：Anacardic酸(AA)是2-hydroxy-6-alkylbenzoic酸相当或相同的事物的混合物。它广泛地被认为是p300的一个非特定的histoneacetyltransferase禁止者。效果和在LNCaP房间(前列腺癌症房间)的AA的机制仍然保持未知。在LNCaP房间上调查AA的效果，我们执行了几个实验并且发现AA禁止LNCaP房间增长，导致G1/S房间周期拘捕和LNCaP的apoptosis房间。AA对LNCaP房间经由起作用的机制可能由于下列方面。首先，AA能除了它在LNCaP房间通过translational以后修正调整p300的功能的机制调整p300抄写和蛋白质水平。第二，AA能通过在LNCaP房间在Ser15上增加p53的phosphorylation激活p53。AA能有选择地激活p21(p53的目标基因)。第三，通过supressingp300的AA罐头下面调整雄激素受体(AR)。我们的学习建议AA在LNCaP房间举办多重反肿瘤活动并且保证进一步的调查。

简介：Objectiveandbackground:Althoughp21rashasbeenreportedtobeupregulatedinhepatocellularcarcinomacomplicatingchronichepatitisCtypeI,p21rashasadifferentroleinadvancedstages,asithasbeenfoundtobedownregulated.Thegoalofthisstudywastoinvestigatethestatusofp21rasinearly-stage/low-gradeandlate-stage/high-gradehepatocellularcarcinomaanditspossiblelinktoapoptosis.Materialandmethods:Thirty-fivecaseseachofchronicHCVhepatitistype4(groupI)andcirrhosiswithhepatocellularcarcinoma(HCC)complicatingchronicHCVhepatitis(groupsIIandIII)wereimmunohistochemicallyevaluatedusingap21raspolyclonalantibody.Theapoptoticindexwasdeterminedinhistologicsectionsusingtheterminaldeoxynucleotidyltransferase-mediatedd-UTPbiotinnickendlabeling(TUNEL)assay.Results:Significantdifferences(P=0.001)weredetectedinp21rasproteinexpressionbetweenthethreegroups.Anear2-foldincreaseinp21rasstainingwasobservedinthecirrhoticcasescomparedtothehepatitiscases,andp21rasexpressionwasdecreasedintheHCCgroup.p21rasexpressioncorrelatedwithstage(r=0.64,P=0.001)andgrade(r=-0.65,P=0.001)intheHCCgroupandgradeintheHCVgroup(r=0.44,P=0.008).Bothp21rasexpressionandTUNEL-LIweresignificantlylowerinlargeHCCscomparedtosmallHCCs(P=0.01each).TheTUNELvalueswerenegativelycorrelatedwithstageintheHCCgroup(r=-0.85,P=0.001).TheTUNELvalueswerealsonegativelycorrelatedwithgradeinboththeHCVandHCCgroups(r=0.89,P=0.001andr=-0.53,P=0.001,respectively).Thep21rasscoresweresignificantlycorrelatedwiththeTUNEL-LIvaluesintheHCCgroup(r=0.63,P=0.001)andHCVgroup(r=0.88,P=0.001).Conclusions:p21rasactsasaninitiatorinHCCcomplicatingtype4chronicHCVandisdownregulatedwithHCCprogression,whichmostlikelypromotestumorcellsurvivalbecauseitfacilitatesthedownregulationofapoptosiswithtumorprogression.