简介：AbstractBackground:Circular RNAs (circRNAs) are endogenous non-coding RNAs, some of which have pathological roles. The current study aimed to explore the role of circRNA BTG3-associated nuclear protein (circ-BANP) binding with let-7f-5p and its regulation of the toll-like receptor 4 (TLR4)/signal transducer and activator of transcription 3 (STAT3) signaling pathway in residual hepatocellular carcinoma (HCC) after insufficient radiofrequency ablation (RFA).Methods:Circ-BANP, let-7f-5p, and TLR4 expressions in HCC samples were assessed using reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and Western blotting. Bioinformatics prediction, RNA pull-down assay, and dual luciferase reporter gene assay were used to analyze the relationships among circ-BANP, let-7f-5p, and TLR4. Huh7 cells were used to generate an in vitro model of residual HCC, defined as Huh7-H cells, which were transfected with either a plasmid or the sequence of circ-BANP, let-7f-5p, or TLR4. Expression of circ-BANP, let-7f-5p, and TLR4 mRNA was determined by RT-qPCR. TLR4, STAT3, p-STAT3, vascular endothelial growth factor A, vascular endothelial growth factor receptor-2, and epithelial-mesenchymal transformation (EMT)-related factors proteins were determined by Western blotting. Cell proliferation was determined by cell counting kit-8 and 5-Ethynyl-2’-deoxyuridine (EdU) assay and cell migration and invasion by Transwell assay. Animal studies were performed by inducing xenograft tumors in nude mice.Results:Circ-BANP and TLR4 mRNAs were upregulated in HCC tissues (the fold change for circ-BANP was 1.958 and that for TLR4 was 1.736 relative to para-tumors) and expression further increased following insufficient RFA (fold change for circ-BANP was 2.407 and that of TLR4 was 2.224 relative to para-tumors). Expression of let-7f-5p showed an opposite tendency (fold change for let-7f-5p in HCC tissues was 0.491 and that in tumors after insufficient RFA was 0.300 relative to para-tumors). Competitive binding of circ-BANP to let-7f-5p was demonstrated and TLR4 was identified as a target of let-7f-5p (P < 0.01). Knockdown of circ-BANP or elevation of let-7f-5p expression inhibited the TLR4/STAT3 signaling pathway, proliferation, invasion, migration, angiogenesis, and EMT in Huh7 and Huh7-H cells (P < 0.01). The effects induced by circ-BANP knockdown were reversed by let-7f-5p inhibition. Overexpression of TLR4 reversed the impact of let-7f-5p upregulation on the cells (P < 0.01). Silencing of circ-BANP inhibited the in vivo growth of residual HCC cells after insufficient RFA (P < 0.01).Conclusions:Knockdown of circ-BANP upregulated let-7f-5p to inhibit proliferation, migration, and EMT formation in residual HCC remaining after insufficient RFA. Effects occur via regulation of the TLR4/STAT3 signaling pathway.

简介：AbstractBackground:The hepatitis B virus X (HBx) protein plays a critical role in the initiation and progression of hepatitis B virus (HBV)-associated hepatocellular carcinoma (HCC). In the early stage of the disease, HBx facilitates tumor onset by inactivating the tumor suppressor p53. The p53-encoding gene, however, is frequently mutated or deleted as the cancer progresses to the late stage and, under such circumstance, the p53 homolog TAp63 can harness HCC growth by transactivating several important p53-target genes.Methods:To determine whether HBx regulates TAp63, we performed co-immunoprecipitation assay, real-time quantitative polymerase chain reaction, immunoblotting, and flow cytometry analysis in p53-null cancer cell lines, Hep3B and H1299.Results:HBx interacts with the transactivation domain of TAp63, as HBx was co-immunoprecipitated with TAp63 but not with ΔNp63. The interaction between HBx and TAp63 abolished transcriptional activity of TAp63, as evidenced by the reduction of the levels of its target genes p21 and PUMA, consequently leading to restricted apoptosis and augmented proliferation of HCC cells.Conclusion:HBV induces progression of HCC that harbors defective p53 by inhibiting the tumor suppressor TAp63.

简介：客观刺猬(HH)的激活小径包括hepatocellular癌(HCC)在人的恶意的发展被含有。然而，在HCC病人的HH激活的临床的影响仍然是不清楚的。这研究被进行证实HH小径部件的表示是否与HCC前进和临床的结果被联系。这研究是的方法一膨胀样品、延长列在后面在上面我们的以前的研究之一。它包括了从2002～2005经历了外科的治疗的46个HCC病人。声音的HH(嘘)的表示，patched-1(PTCH1)，smoothened(SMOH)和在肿瘤和邻近的正常纸巾的基因从病人提取了的联系glioma的oncogene-1(GLI1)被反向的transcriptionpolymerase链反应(RT-PCR)检验探索在这些基因和HCC的临床的预后之间的关系。表示在HCC纸巾嘘，PTCH1，SMOH和GLI1铺平的结果分别地是60.87%，50.00%，32.61%和54.35%。嘘相关的分子的表示层次在癌症织物是相对强烈的，但是不足道与肿瘤的任何clinicopathological因素相关。Transcriptional因素GLI1是在HCC病人之中与差的预后联系的唯一的分子。在肿瘤纸巾的GLI1基因的表示显著地与没有疾病的幸存(DFS)(P=0.042)和全面幸存(OS)(P=0.030)被联系。在肿瘤和邻近的正常的肝纸巾的GLI1的同时的表示与DFS相关(P<0.029)并且OS(P<0.025)。结论HH发信号激活是在人的HCC的发展的一个重要事件。在嘘小径的GLI1的表示可能涉及HCC前进，它可以是HCC的有用预示的指示物。

简介：Objective:ToinvestigatetheexpressionofE2FandBcl-2andtheclinicopathologicalsignificanceinhepatocellularcarcinoma.Methods:TheexpressionsofE2F-3andBcl-2in74patientswithhepaticcarcinoma,paracarcinomaand15patientswithlivercirrhosisweredetectedbyS-Pimmunohistochemicalstaining.Results:TheexpressionofE2Finhepaticcarcinomawassignificantlyhigherthanthatinparacarcinomaorlivercirrhosis(P<0.005),theexpressionofBcl-2inhepaticcarcinomawassignificantlyhigherthanthatinparacarcinoma(P<0.005),inwhichBcl-2expressionwaslowerthaninlivercirrhosis(P<0.05).TheexpressionofE2F-3wasrelatedwithhistologicalgrade,tumorsize,andtheexpressionofBcl-2wasrelatedwithhistologicalgrade,tumorsizeandtumornumber.TherewascorrelationbetweentheexpressionofE2F-3andBcl-2inhepaticcarcinoma.Conclusion:E2F-3andBcl-2expressionmayplayanimportantroleindevelopment,progressionandcellapoptosisoftumor.

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：Objective:TheexpressionofB-celllymphoma2(Bcl-2)seemstobeinfluencedbytheendocrineenvironment.NumerousreportsdemonstratethediverseexpressionofBcl-2familymembersundersexsteroidregulation.Withtheexceptionofestrogen-relatedtumors,androgen-relatedtumorshaveshowntheircharacteristicsinBcl-2expression.Inthisstudy,thestatusofBcl-2expressioninmalehepatocellularcarcinoma(HCC)patientswasexaminedtoverifythehighincidenceofHCCinmales.Methods:TumortissuemicroarraywasusedtoexamineBcl-2expressionlevelsin374HCCcasesincluding306malesand68females.Kaplan-Meiermethod,log-ranktest,andCoxproportionalhazardsmodelwereappliedtoinvestigatethepredictivevalueofBcl-2inHCCpatients.Results:ImmunohistochemistryanalysisshowedthatmalepatientswithhigherBcl-2levelshadsignificantlylongermediansurvivaltimeandrecurrencetimethanthosewithlowerlevels.However,nosignificantdifferencesinoutcomeswerefoundbetweendifferentBcl-2levelsinfemalepatients.Whenthemalepatientswerestratifiedintoseveralagepoints,thelevelofBcl-2expressionshowedpoorerpredictiveefficiencyinthe45–49and55–60agegroupsinandropause-agepatientscomparedwithotheragegroups.Bcl-2wasanindependentprognosticfactorforbothoverallsurvival(P<0.0001)andrecurrencetime(P=0.0001)inmalepatients.Afterexcludingmalepatientsinthe45–60agegroup,thepredictiveefficiencywasenhanced(n=147,OS,P=0.0002,TTR,P<0.0001).Conclusions:Bcl-2expressionisanindependentpredictorofsurvivalandrecurrenceinmaleHCC.Bcl-2levelsmayalsoberegulatedbyandrogensorandrogenreceptorsinmaleHCCpatients.Bcl-2levelschangeandexhibitpoorpredictiveefficiencywhenandrogenlevelsvarydramatically(andropauseage).

简介：Apoptosisplaysanimportantroleinembryonicdevelopment,tissueremodeling,immuneregulationandtumorregression.Twogroupsofmolecules(Bcl-2familyand“Deathfactor”family)areinvolvedinregulatingapoptosis.InordertoknowabouttheeffectofBcl-2onapoptosisinducedbyFas,atypicalmemberof“Deathfactor”family,thetransfectionexperimentswithexpressionvectorspcDNA3-flandpcDNA3-bcl-2wereperformedinBEL-7404cells,ahumanhepatocellularcarcinomacelllinewhichexpressesendogenousFas,butnotFasLandBcl-2.ThedatashowedthattheexpressionofFasLinpcDNA3-fltransfectedhepatomacellsobviouslyinducedtheapoptosisofthecells.However,theoverexpressionofBcl-2inpcDNA3-bcl-2transfected7404/b-16cellscounteractedpcDNA3-fltransienttransfectionmediatedapoptosis.FurtherstudybycotransfectionexperimentsindicatedthatBidbutnotBax(bothwerepro-apoptoticproteinsofBcl-2family)blockedtheinhibitoryeffectofBcl-2onFas-mediatedapoptosis.TheseresultssuggestedthatFas-mediatedapoptosisinhumanhepatomacellsispossiblyregulatedbyBcl-2familyproteinsviamitochondriapathway.

简介：瞄准：在主要hepatocellular癌(HCC)探索E2F5的表示模式并且阐明在hepatocarcinogenesis的E2F5的角色。方法：E2F5表示被immunohistochemistry分析在120主要HCC和29正常的肝纸巾分析。E2F5小的介入RNA是进HepG2的transfected，一根E2F5-overexpressedHCC房间线。在E2F5以后击倒，细胞生长能力和移居的潜力被检验。结果：E2F5是显著地在主要HCC的overexpressed与正常的肝纸巾相比(P=0.008)。显著地显示出的沉默E2F5的房间减少了增长(P=0.004)。在殖民地形成和软琼脂试金上，殖民地的数字显著地在沉默E2F5的房间被减少(P=0.004并且P=0.009，分别地)。E2F5击倒导致了G0/G1阶段房间和S阶段房间的减小的累积。移居/入侵房间的数字也在E2F5以后被减少击倒(P=0.021)。结论：到我们的知识，这是E2F5是的第一条证据通常在主要HCC和那E2F5的overexpressed击倒显著地镇压了HCC房间的生长。

简介：调查瘤的目的淋巴的联系转移的基因；它的分子的机制。方法22690鼠标染色体cDNA微数组(包括14500知道基因；4371EST)被用来比较；分析老鼠肝细胞癌房间线Hca-F(高度淋巴的转移潜力)的基因表示侧面；Hca-P(低潜力)。结果901基因；129EST至少是起来调整的在Hca-F的2褶层房间。在表示显示出重要改变的33基因被介绍，包括endoglin(EDG)，MCAM，Cdc42ep5，F2r，D7Ertd458e，Serpinh1(HSP47)，AXL，Areg；那么上。这些基因有血管生成的函数，房间粘附，信号转导变异，房间活动性，女伴活动，蛋白质激酶活动；受体绑定。微数组与淋巴的转移模型相结合的结论cDNA可能贡献新方法；淋巴的转移研究的瘤的线索。在表示基因上的一些可能提供新奇线索给瘤的分子的机制淋巴的转移。

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简介：AIM:Todeterminetheexpressionsofinduciblenitricoxidesynthase(iNOS)andmatrixmetalloproteinase-9(MMP-9)inhepatocellularcarcinoma(HCC)andtoinvestigatetherelationshipbetweeniNOSandMMP-9expressionandtheireffectsonangiogenesisandprogressionofHCC.METHODS:Tnthisstudy,weexaminediNOS,MMP-9,andCD34expressioninspecimenssurgicallyremovedfrom32HCCpatientsand7normallivertissuesbyimmunohistochemicalstaining.Meanwhile,microvesseldensity(MVD)wasdeterminedasamarkerofangiogenesisbycountingCD34-positivecells.RESULTS:ThepositiveratesofiNOSandMMP-9expressionwere71.88%(23/32)and78.13%(25/32)inHCC.MMP-gexpressionwassignificantlycorrelatedwithtumorsize,capsulestatus,TNMstage,andriskofHCCrecurrence(P=0.032,P=0.033,P=0.007,andP=0.001,respectively).TherewasalsoasignificantrelationshipbetweeniNOSexpressionandcapsulestatusandriskofHCCrecurrence(P=0.04gandP=0.004,respectively),butnocorrelationbetweeniNOSexpressionandtumorsizeandTNMstage.TherewasapositiveassociationbetweenMVDandTNMstageandriskofHCCrecurrence(P=0.037andP=0.000,respectively).ThecountofMVDwassignificantlydifferentindifferentiNOSandMMP-9immunoreactivitygroups(F=17.713and17.097,P=0.000andP=0.000,respectively).TheexaminationofSpearman'srankcorrelationcoefficientshowedthattherewasasignificantpositivecorrelationbetweenMVDandiNOS,MMP-9immunoreactivity(r=0.754and0.751,P=0.000andP=0.000,respectively).TherewasalsoasignificantassociationbetweenMMP-9andiNOSexpressioninHCC(P=0.010).CONCLUSION:Nitricoxide(NO)producedbyiNOScouldmodulateMMP-9productionandthereforecontributetotumorcellangiogenesisandinvasionandmetastasisinHCC.ThestrongexpressionofiNOSandMMP-9inHCCmaybehelpfulinevaluatingtherecurrenceofHCC,predictingpoorprognosis.ForpatientswithstrongexpressionofMMP-9andiNOS,theoptimaltreatmentschemen

简介：AbstractBackground:To determine the prevalence and prognostic impact of hepatopulmonary syndrome (HPS) in patients with unresectable hepatocellular carcinoma (HCC) undergoing transarterial chemoembolization (TACE).Methods:Fifty-four patients with unresectable HCC undergoing TACE between December 2014 and December 2015 were prospectively screened for HPS and were followed up for a maximum of 2 years or until the end of this prospective study.Results:Nineteen of the 54 (35.2%) patients were considered to have HPS, including one (5.3%) with severe HPS, nine (47.4%) with moderate HPS, and nine (47.4%) with mild HPS. The median overall survival (OS) was 10.1 (95% confidence interval [CI], 3.9–16.3) months for patients with HPS and 15.1 (95% CI, 7.3–22.9) months for patients without HPS, which is not a significant difference (P = 0.100). The median progression-free survival was also not significantly different between patients with and without HPS (5.2 [95% CI, 0–12.8] vs. 8.4 [95% CI, 3.6–13.1] months; P = 0.537). In the multivariable Cox regression analyses, carbon monoxide diffusing capacity (hazard ratio [HR] = 1.033 [95% CI, 1.003–1.064]; P = 0.028) and Child-Pugh class (HR = 1.815 [95% CI, 1.011–3.260]; P = 0.046) were identified to be the independent prognostic factors of OS.Conclusion:Mild or moderate HPS is common in patients with unresectable HCC undergoing TACE, but it does not seem to have a significant prognostic impact.

简介：Objective:Spontaneoushepatocellularcarcinoma(HCC)rupturecanbefatal,andhepaticresectioncouldachieveafavorablelong-termsurvivalamongallstrategiesoftumorrupture.However,thereisnoavailableprognosticscoringsystemforpatientswithrupturedHCCwhounderwentpartialhepatectomy.Methods:FromJanuary2005toMay2015,129patientswithspontaneousHCCruptureunderwentpartialhepatectomy.Preoperativeclinicaldatawerecollectedandanalyzed.Independentriskfactorsaffectingoverallsurvival(OS)wereusedtodevelopthenewscoringsystem.Harrell'sCstatistics,Akaikeinformationcriterion(AIC),therelativelikelihood,andtheloglikelihoodratiowerecalculatedtomeasurethehomogeneityanddiscriminatoryabilityofaprognosticsystem.Results:InthemultivariableCoxregressionanalysis,threefactors,includingtumorsize,preoperativeα-fetoproteinlevel,andalkalinephosphataselevel,werechosenforthenewtumor-associatedantigen(TAA)prognosticscoringsystem.The1-yearOSrateswere88.1%,43.2%,and30.2%forTAAscoresof0-5points(low-riskgroup),6-9points(moderate-riskgroup),and10-13points(high-riskgroup),respectively.TheTAAscoringsystemhadsuperiorhomogeneityanddiscriminatoryability(Harrell'sCstatistics,0.693vs.0.627and0.634;AIC,794.79vs.817.23and820.16;relativelikelihood,both<0.001;andloglikelihoodratio,45.21vs.22.77and21.84)thantheBarcelonaClinicLiverCancerstagingsystemandtheCanceroftheLiverItalianPrograminpredictingOS.Similarresultswerefoundwhilepredictingdisease-freesurvival(DFS).Conclusions:ThenewprognosticscoringsystemissimpleandeffectiveinpredictingbothOSandDFSofpatientswithspontaneousrupturedHCC.

简介：Hepatocellularcarcinoma(HCC)isoneofthemostdeadlyhumancancers,butitisverydifficulttoestablishananimalmodelbyusingsurgicalspecimens.Inthepresentexperiment,histologicallyintactfreshsurgicalspecimensofHCCweresubcutaneouslytransplantedinnon-obesediabetic/severecombinedimmunodeficienccy(NOD/SCID)mice.Thebiologicalcharacteristicsoftheoriginalandthecorrespondingtransplantedtumorsandcelllineswereinvestigated.Theresultsshowedthat5newanimalmodelsand2primarycelllinesweresuccessfullyestablishedfromsurgicalspecimens.Hematoxylin-eosinstainingshowedthatxenograftsretainedmajorhistologicalfeaturesoftheoriginalsurgicalspecimens.Thetwonewcelllineshadbeencultivatedfor3yearsandsuccessivelypassagedformorethan100passagesinvitro.Themorphologicalcharacteristicsandbiologicfeaturesofthetwocelllinesweregeneticallysimilartotheoriginaltumor.Thesubcutaneoustransplantanimalmodelswithhistologicallyintacttumortissueandprimarycelllinescouldbeusefulforinvivoandinvitrotestingofanti-cancerdrugsandbeidealmodelstostudyvariousbiologicfeaturesofHCC.

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简介：AbstractSurgical resection (SR) is recommended as a radical procedure in the treatment of hepatocellular carcinoma (HCC). However, postoperative recurrence negatively affects the long-term efficacy of SR, and preoperative adjuvant therapy has therefore become a research hotspot. Some clinicians adopt transcatheter arterial chemoembolization (TACE) as a preoperative adjuvant therapy in patients undergoing SR to increase the resection rate, reduce tumor recurrence, and improve the prognosis. However, the findings of the most relevant studies remain controversial. Some studies have confirmed that preoperative TACE cannot improve the long-term survival rate of patients with HCC and might even negatively affect the resection rate. Which factors influence the efficacy of preoperative TACE combined with SR is a topic worthy of investigation. In this review, existing clinical studies were analyzed with a particular focus on several topics: screening of the subgroups of patients most likely to benefit from preoperative TACE, exploration of the optimal treatment regimen of preoperative TACE, and determination of the extent of tumor necrosis as the deciding prognostic factor.

简介：Objective:Multiplemechanismsunderlyingthedevelopmentofportalveintumorthrombus(PVTT)inhepatocellularcarcinoma(HCC)havebeenreportedrecently.However,theoriginsofPVTTremainunknown.Increasingmulti-omicsdataonPVTTsinHCCshavemadeitpossibletoinvestigatewhetherPVTTsoriginatefromthecorrespondingprimarytumors(Ts).Methods:TheclonalrelationshipbetweenPVTTsandtheircorrespondingprimaryTswasinvestigatedusingdatasetsdepositedinpublicdatabases.OneDNAcopynumbervariationsdatasetandthreegeneexpressiondatasetsweredownloadedfortheanalyses.ClonalityanalysiswasperformedtoinvestigatetheclonalrelationshipbetweenPVTTsandTsfromanindividualpatient.DifferentialgeneexpressionanalysiswasappliedtoinvestigatethegeneexpressionprofilesofPVTTsandTs.Results:Oneoutof19PVTTshadnoclonalrelationshipwithitscorrespondingT,whereastheothersdid.ThePVTTswithindependentclonaloriginshoweddifferentgeneexpressionandenrichmentinbiologicalprocessesfromtheprimaryTs.Basedontheuniquegeneexpressionprofiles,agenesignatureincluding24geneswasusedtoidentifypairsofPVTTsandprimaryTswithoutanyclonalrelationship.ValidationinthreedatasetsshowedthatthesetypesofpairsofPVTTsandTscanbeidentifiedbythe24-genesignature.Conclusions:OurfindingsshowadirectevidenceforPVTToriginandconsolidatetheheterogeneityofPVTTsobservedinclinic.TheresultssuggestthatPVTTinvestigationatamolecularlevelisclinicallynecessaryfordiagnosisandtreatment.

简介：AbstractBackground:Pre-operative non-invasive histological evaluation of hepatocellular carcinoma (HCC) remains a challenge. Tumor perfusion is significantly associated with the development and aggressiveness of HCC. The purpose of the study was to evaluate the clinical value of quantitative liver perfusion parameters and corresponding histogram parameters derived from traditional triphasic enhanced computed tomography (CT) scans in predicting histological grade of HCC.Methods:Totally, 52 patients with HCC were enrolled in this retrospective study and underwent triple-phase enhanced CT imaging. The blood perfusion parameters were derived from triple-phase CT scans. The relationship of liver perfusion parameters and corresponding histogram parameters with the histological grade of HCC was analyzed. Receiver operating characteristic (ROC) curve analysis was used to determine the optimal ability of the parameters to predict the tumor histological grade.Results:The variance of arterial enhancement fraction (AEF) was significantly higher in HCCs without poorly differentiated components (NP-HCCs) than in HCCs with poorly differentiated components (P-HCCs). The difference in hepatic blood flow (HF) between total tumor and total liver flow (ΔHF = HFtumor -HFliver) and relative flow (rHF = ΔHF/HFliver) were significantly higher in NP-HCCs than in P-HCCs. The difference in portal vein blood supply perfusion (PVP) between tumor and liver tissue (ΔPVP) and the ΔPVP/liver PVP ratio (rPVP) were significantly higher in patients with NP-HCCs than in patients with P-HCCs. The area under ROC (AUC) of ΔPVP and rPVP were both 0.697 with a high sensitivity of 84.2% and specificity of only 56.2%. The ΔHF and rHF had a higher specificity of 87.5% with an AUC of 0.681 and 0.673, respectively. The combination of rHF and rPVP showed the highest AUC of 0.732 with a sensitivity of 57.9% and specificity of 93.8%. The combined parameter of ΔHF and rPVP, rHF and rPVP had the highest positive predictive value of 0.903, and that of rPVP and ΔPVP had the highest negative predictive value of 0.781.Conclusion:Liver perfusion parameters and corresponding histogram parameters (including ΔHF, rHF, ΔPVP, rPVP, and AEFvariance) in patients with HCC derived from traditional triphasic CT scans may be helpful to non-invasively and pre-operatively predict the degree of the differentiation of HCC.

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简介：AbstractBackground:MicroRNA-20a (miR-20a) is dysregulated in many types of malignancies, including human hepatocellular carcinoma (HCC), but its expression level and functional significance in HCC are still disputed. We aimed to study the role of miR-20a-5p in HCC and its downstream molecular mechanisms.Methods:We used real-time polymerase chain reaction to detect the expression of miR-20a-5p and runt-related transcription factor 3 (RUNX3) in HCC and paraneoplastic tissue, transfected Huh7 and highly metastatic human hepatocellular carcinoma (MHCC97H) cells. A live cell workstation was used to observe the proliferation and migration of transfected cells. The invasiveness of transfected cells was verified by Transwell assay. Cell apoptosis was detected by flow cytometry. The expression levels of proteins after transfection were measured using simple western immunoblot measurements. Gene expression profiles between HCC and normal samples were obtained from The Cancer Genome Atlas. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment results were processed by the database for annotation, visualization and integrated discovery. Potential target genes of miR-20a-5p were predicted to further investigate how miR-20a-5p regulates epithelial-mesenchymal transition (EMT) in HCC.Results:MiR-20a-5p was significantly highly expressed in HCC tissues, and overexpression of miR-20a-5p significantly promoted HCC cell proliferation, migration, and invasion and inhibited apoptosis in vitro. The protein expression of E-cadherin was decreased and that of vimentin was increased after overexpression of miR-20a-5p in HCC cells. We discovered the intersection of genes from miRDB, miR TarBase, and TargetScan, obtained 397 target genes and finally focused on RUNX3. RUNX3 was not only reduced in HCC specimens but also drastically reduced in HCC cells overexpressing miR-20a-5p. RUNX3 expression decreased with elevated miR-20a-5p, which activated downstream EMT signaling and promoted cell proliferation, migration, and invasion.Conclusions:Since RUNX3 is involved in EMT in HCC, as proven by previous research, our findings provide further evidence for a novel regulatory pathway comprising the miR-20a/RUNX3/EMT axis that upregulates EMT signaling and enhances the migration of HCC cells.