简介：变形癌症房间的俘获和察觉为恶意的瘤的诊断和治疗是关键的。这里，我们报导folic酸(FA)的使用poly修改了electrospun(乙烯基白酒)(PVA)为癌症房间俘获应用的/polyethyleneimine(PEI)nanofibers。由glutaraldehyde蒸汽的ElectrospunPVA/PEInanofiberscrosslinked与FA被修改经由一poly(乙烯乙二醇)(木钉)分隔符，由纤维表面PEI胺的acetylation列在后面。形成的修改FA的nanofibers很好被描绘。electrospunPVA/PEInanofibers的形态学尽管有表面修正光滑、一致。另外，修改FA的nanofibers显示由溶血证实了的好hemocompatibility试金。重要地，发达修改FA的nanofibers能明确地捕获癌症房间overexpressingFA受体，它被数试金和质的共焦的显微镜学分析的量的房间验证。发达修改FA的PVA/PEInanofibers可以被用于为癌症诊断应用程序捕获传播肿瘤房间。

简介：有干细胞特征的前列腺癌症房间被他们在非支持者文化从单个房间形成自我更新的prostaspheres的能力在人的前列腺癌症房间线识别。Prostaspheres展出了增长，区别和茎的异构的表示联系房间的制造者CD44，ABCG2和CD133。有WNT禁止者的治疗减少了prostasphere尺寸和自强。相反，引起的Wnt3a的增加增加了prostasphere尺寸和自强，它与原子尾-catenin的重要增加被联系，角质素18，CD133和CD44表示。作为LNCaP和C4-2B癌症房间快车雄激素受体的一个高比例，我们决定了雄激素受体对手bicalutamide的效果。雄激素受体抑制减少了prostasphere尺寸和PSA的表示，但是没禁止prostasphere形成。这些效果与有干细胞特征和放大房间的运输的雄激素依赖者增长的房间的雄激素无关的自强一致。作为发信号的受动器尾-catenin能也与雄激素受体联系的正规WNT，我们为包含在WNT和雄激素受体活动之间的平衡的瘤繁殖建议一个模型。那将与干细胞特征和开车运输放大房间增长和区别影响一个癌症房间的自强。在结论，我们提供那项WNT活动独立于雄激素受体活动与干细胞特征调整前列腺癌症房间的自强的证据。WNT发信号的抑制因此有潜力与干细胞特征减少前列腺癌症房间的自强并且改进治疗学的结果。

简介：Objective:Avarietyofionchannelshavebeenimplicatedinbreastcancerproliferationandmetastasis.VoltagegatedK+(Kv)channelsnotonlycauserepolarizationinexcitablecells,butarealsoinvolvedinmultiplecellularfunctionsinnon-excitablecells.InthisstudyweinvestigatedtheroleofKvchannelsinmigrationofBT474breastcancercells.Methods:Transwelltechniquewasusedtoseparatemigratorycellsfromnon-migratoryonesandthesetwogroupsofcellsweresubjecttoelectrophysiologicalexaminationsandmicrofluorimetricmeasurementsforcytosolicCa2+.CellmigrationwasexaminedintheabsenceorpresenceofKvchannelblockers.Results:Whencomparedwithnon-migratorycells,migratorycellshadmuchhigherKvcurrentdensities,butratherunexpectedly,moredepolarizedmembranepotentialandreducedCa2+influx.Reversetranscriptasepolymerasechainreaction(RT-PCR)analysisrevealedthepresenceofKv1.1,Kv1.3,Kv1.5,Kv2.1,Kv3.3,Kv3.4andKv4.3channels.Cellmigrationwasmarkedlyinhibitedbytetraethylammonium(TEA),adelayedrectifierKvchannelblocker,butnotby4-aminopyridine,anA-typeKvchannelblocker.Conclusions:Takentogether,ourresultsshowthatincreasedKvchannelexpressionplayedaroleinBT474cellmigration,andKvchannelscouldbeconsideredasbiomarkersorpotentialtherapeutictargetsforbreastcancermetastasis.Themechanism(s)bywhichKvchannelsenhancedmigrationappearedunrelatedtomembranehyperpolarizationandCa2+influx.

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简介：AbstractBackground:The first-line treatment for lung cancer is surgical resection, and one-lung ventilation (OLV) is the most basic anesthetic management method in lung surgery. During OLV, inflammatory cytokines are released in response to the lung tissue damage and promote local and contralateral lung damage through the systemic circulation. We designed a randomized, prospective study to evaluate the effect of the urinary trypsin inhibitor (UTI) ulinastatin on the inflammatory response after video-assisted thoracic lobectomy in patients with lung cancer.Methods:Adult patients aged 19 to 70 years, who were scheduled for video-assisted thoracic lobectomy surgery to treat lung cancer between May 2020 and August 2020, were enrolled in this randomized, prospective study. UTI (300,000 units) mixed with 100 mL of normal saline in the ulinastatin group and 100 mL of normal saline in the control group was administered over 1 h after inducing anesthesia.Results:The baseline (T0) interferon-γ (IFN-γ)/interleukin-4 (IL-4) ratio was not different between the groups (6941.3 ± 2778.7 vs. 6954.3 ± 2752.4 pg/mL, respectively; P > 0.05). The IFN-γ/IL-4 ratio was significantly higher in ulinastatin group at 30 min after entering the recovery room than control group (20,148.2 ± 5054.3 vs. 6674.0 ± 2963.6, respectively; adjusted P < 0.017). Conclusion: Administering UTI attenuated the anti-inflammatory response, in terms of INF-γ expression and the IFN-γ/IL-4 ratio, after video-assisted thoracic surgery in lung cancer patients.Trial registration:Clinical Research Information Service of Korea National Institute of Health (CRIS), KCT0005533.

简介：ObjectToexploretileeffectoflipofectin-c-erbB2antisenseoligodeoxynucleotidesonradiosensitivityofhumanovariancancercellllne.MethodsTheexpressionofc-erbB2wasdetectedbymeansofRT-PCR,cellularresponsetoirradiationwasevaluatedbytilecolonyformingassay.ResultsLipofectin-c-erbB2antisenseoligodeoxynucleotides（AS-ODN)couldsuppresstheexpressionofc-erbB2,andsignificantlydecreasedthecolonyformingrateofhumanovariancancercellsafterionizingirradiation（P<0.01),whilenon-trean~entandthesenseoligodeoxynucleotides{S-ODN)groupsdidnotdecreaseontheradio-resistancelevelofSKOV3cellline{P>0.05).Condusionc-erbB2antisenseoligodeoxynueleotidessensitizedtheSKOV3toionizingirradiationthroughdecreasingtheexpressionofe-erbB2,whichmightbetheresultofthefactthatc-erbB2antisenseoligodeoxynueleotidesinhibittheeelluarsignaltransductionpathwayrelatingtotheradiation-resistantphenotype.

简介：一些研究证明了三角洲Np63的损失与好攻击的显型和差的预后被联系。然而，另外的研究显示三角洲Np63被认为有oncogenic性质。三角洲Np63overexpression经常与有鳞的房间癌和膀胱癌症的oncogenic生长联合被观察。在这研究，我们在在膀胱(TCCB)的过渡房间癌调整房间粘附调查了三角洲Np63的oncogenic角色。房间是稳定地有三角洲Np63短发卡RNA(shRNA)plasmid的transfected。Immunocytochemistry被执行决定击倒的效率。瘤房间为他们遵守脉管的endothelial房间的能力被学习。共焦的显微镜学被用来在细胞骨架F肌动朊分析变化。F肌动朊表示被流动cytometry测量。房间侵略能力用transwell房间被估计。沉默Np63的瘤房间被显示出比控制更紧粘住到脉管的endothelial房间的三角洲(P<；0.05)。在三角洲的F肌动朊的内容沉默Np63的房间被提高(P<；0.05)。当时，Matrigel侵略试金证明人5637膀胱癌症房间有活动性的更低的度有pdeltaNp63-shRNA的transfected(P<；0.05)。在结论，三角洲Np63表示的silencing能由导致F肌动朊细胞骨架生产提高5637个房间的粘着性，并且它将可能禁止TCCB侵略和转移。

简介：Objective:ToinvestigatetheantitumoractivityandthemechanismofBRM-SJSonbreastcancercells.Methods:Flowcytometry,DNAagarosegelelectrophoresisandothertechniqueswereusedtostudytheinvitroandinvivoinhibitoryeffectonBcaP-37cellsbyBRM-SJS.Results:BRM-SJSshowedaninhibitoryrateof33.8%oninvivotransplantedtumor(P<0.05,comparedwithcontrol).TheflowcytometryanalysisofBRM-SJStreatedBcaP-37(2.5μmol/L,5μmol/L,10μmol/Lfor48hand72h)revealedtypicalsub-G1peak.ThespecificDNALadderswereexhibitedwithBRM-SJSBcaP-37cellstreated.Conclusion:BRM-SJShasmarkedantitumoractivityonBcaP-37anditsinhibitoryeffectsontumorwererealizedbybothinductionofapoptosisandnecrosisofthetumorcells.

简介：94氨基酸(PSP94)的能分泌的蛋白质被显示出与充满半胱氨酸的能分泌的蛋白质交往的前列腺3(CRISP-3)在里面人的精液的血浆。有趣地，PSP94表示被减少或在前列腺瘤的多数输了，而CRISP-3表示与正常前列腺织物相比是在前列腺癌症的upregulated。为了获得单个角色的更好的理解，这些蛋白质在前列腺tumourigenesis和他们的相互作用的功能的关联有，我们宫外地在三根前列腺细胞线(PC3，WPE1-NB26和LNCaP)与CRISP-3一起表示了PSP94或PSP94并且执行了生长抑制试金。反向的抄写聚合酶链反应和西方的污点分析被用来为PSP94和CRISP-3表示屏蔽前列腺房间线。为人的PSP94和CRISP-3的哺乳动物的表示构造也被产生，recombinant蛋白质的表示，本地化和分泌物是由西方的污点分析和immunofluorescence试金跟随的transfection的assayed。PSP94或CRISP-3的宫外的表示在房间生长上有的效果被clonogenic幸存试金追随者transfection学习。评估二蛋白质的合作表示的效果，表示了PSP94的PC3的稳定的克隆被产生。他们是随后有CRISP-3表示构造的transfected并且使遭到了到clonogenic幸存试金。我们的结果证明PSP94和CRISP-3能各在一根细胞线导致生长抑制特定的举止。尽管CRISP-3-positive房间线的生长被PSP94禁止，生长抑制由CRISP-3调停了没被PSP94的存在或缺席影响。这建议CRISP-3可以在前列腺tumourigenesis期间参予PSP94独立的活动。

简介：瞄准：由一个树枝状的房间(DC)调查反肿瘤免疫鼠科的前列腺癌症上的疫苗的编码第二等的淋巴的chemokine基因和肿瘤lysate。方法：从C57BL/6的骨头髓的DC是有表示第二等的淋巴的chemokine(SLC)的原生质标志向量的transfected由Lipofectamine2000的cDNA脂肪的一些和肿瘤lysate。从SLC+lysateDC提取的全部的RNA被用来由反向的transcriptase聚合酶链反应(RT-PCR)验证SLC的表示。免疫在鼠科的前列腺癌症上疫苗的DC的治疗学的效果被估计。结果：当与SLC相比DC，lysateDC，DC或磷酸盐缓冲答案(PBS)时，我们发现在C57BL/6鼠标的前列腺肿瘤模型，SLC+lysateDC的adminstration最显著地禁止了肿瘤生长对应物(P<0.01)。荧光灯的染色分析显示出的Immunohistochemical在确定的肿瘤以内的更多的CD4+,CD8+T房间和CD11c+DC的渗入由比另外的DC疫苗疫苗的SLC+lysateDC对待(P<0.01)。结论：编码第二等的淋巴的chemokine和肿瘤lysate的DC疫苗能由CD4+,CD8+T房间和DC的渗入得到重要的反肿瘤免疫，它可能为前列腺癌症提供一个潜在的免疫疗法方法。

简介：免疫疗法和化疗的联合为癌症的某些类型的治疗被认为是一条有希望的途径。然而，内在的机制需要充分被调查为癌症chemoimmunotherapy指导更有效的协议的设计。联系危险的分子的模式(阻尼)能激活有免疫力的房间，是众所周知的，包括树枝状的房间(DC)，经由像使用费的受体(TLR)；然而，在有免疫力的反应的激活免除化学对待药的肿瘤房间的阻尼的角色需要进一步被阐明。这里，我们发现那colorectal与oxaliplatin(OXA)对待的癌症(CRC)房间或5氟尿嘧啶(5-Fu)释放了高活动性的组盒子1的高水平(HMGB1)和热吃惊蛋白质70(HSP70)。在OXA/5-Fu治疗以后，也展出的CRC病人的sera增加了HMGB1和HSP70的层次，哪个是著名阻尼。与OXA/5-Fu对待的垂死的CRC房间的上层清液支持了老鼠和人的DC成熟，与HLA医生，CD80和CD86表示和IL-1β的改进的upregulation；，TNF-α；，MIP-1α；，MIP-1β；，RANTES和IP-10生产。由DC组成的疫苗与导致的化学上强调的CRC房间的上层清液搏动了更重要的IFN-γ；在vitro并且在vivo生产Th1反应。然而，化学上强调的CRC房间的上层清液没能在TLR4缺乏的DC导致phenotypic成熟和cytokine生产，显示在导致阻尼的DC成熟和激活的TLR4的一个必要角色。而且，有化学上强调的CRC房间的上层清液的pulsing高效地没导致IFN-γ；在TLR4缺乏的DC生产Th1反应。一起，这些结果证明免除化学上强调的癌症房间的阻尼能经由TLR4激活DC并且提高反肿瘤T房间有免疫力的回答的正式就职，描出一条临床上相关的免疫助手小径由阻尼被触发。

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简介：Objective:Toinvestigatethetreatmentofspontaneousmetastaticlungcancerbytumorantigen-pulsed,interleukin-12(IL-12)gene-modifieddendriticcells(DC).Methods:Thespontaneousmetastaticlungcancermodel,preparedbyinjectionofthe3LLLewislungcancercellsintothefootpadsofC57BL/6mice,wastreatedbysubcutaneousvaccinationwithtumorantigenpeptidemut1-pulsed,IL-12gene-modifieddendriticcells(DC-IL-12/mut1)derivedfromthenormalbonemorrow.Aftertreatment,thelungweight,thenumberoflungmetastaticnodesandthesurvivaltimeofthetumor-bearingmicewereobserved,andtheNKandCTLactivityweredeterminedrespectively.Themiceweredividedinto8groupswith12miceineachgroup.Results:Comparedwithmicetreatedwithmut1-pulsed,controlLacZgenemodifiedDCanduntreatedDC,tumor-bearingmicetreatedwithDC-IL-12/mut1hadthelightestlungweights(P<0.01),theleastlungmetastaticnodenumber(P<0.01),thelongestsurvivaltime(P<0.01),alsowiththeinductionofpotentCTLactivity(P<0.01)andNKactivity(P<0.01).Conclusion:Tumorantigen-pulsed,IL-12gene-modifieddendriticcellshavesignificanttherapeuticeffectsonthespontaneousmetastaticlungcancer,providinganewapproachtotreatmentoflungtumors.

简介：为排干肿瘤的淋巴的刺激发现一个可行方法为在诊所的使用作准备的节点(TDLN)房间，TDLN房间的CTL活动由不同刺激导致了(IL-2独自一个，IL-2+自体同源的肿瘤抗原(atAg)，IL-2+GM-CSF+IL-4+atAg)被最大的LDH测量酶版本。机制被形态学和CD83+TDLN房间的察觉的观察探索。由IL-2+GM-CSF+IL-4+atAg的TDLN房间的扩大由独自一个的IL-2或IL-2+atAg比那显著地高(p<0.01)。IL-2+GM-CSF+IL-4+atAg导致的TDLN房间的AntitumorCTL活动比另外的组的那些显著地高。在与IL-2+GM-CSF+IL-4+atAg对待的TDLN人口以内的CD83+房间的数字显著地被提高。由IL-2+GM-CSF+IL-4+atAg刺激TDLN房间的方法比有IL-2或IL-2+atAg的刺激好。IL-2+GM-CSF+IL-4+atAg导致的TDLN房间生产了更树枝状的房间(DC)。在我们的学习，我们建立了T房间和DC一起被刺激的一个系统前vivo，它是容易的进行并且生产有希望的结果。它为改进可能在临床的癌症治疗被使用的TDLN房间antitumor活动提供了一个新方法。

简介：FivehundredsandfiftyLACAmicewereusedin3batchesforstudyingtheanticarcinogeniceffectofKonjakupowderonMNNG-inducedlungcancers.Thesemice(withineachbatch)wererandomlyallocatedtofourgroups,namely,positivecontrol(MNNG),Amorphophalluskonjac(A.K.),complex(MNNG+A.K.),andblankcontrol(C)group.InMNNGgroup,MNNG(250μg)wasinjectedintravenouslyoncefivedaysforseventimesineachmouse,thetotaldosageofMNNGbeing1.75mk.InA.K.group,accordingtow/w,8%A.K.waswellmixedinto92%commondietforlong-termbreeding.Incomplexgroup,MNNGwasgivenasthatinMNNGgroupandthemicewererearedasthoseinA.K.group.ThemiceinMNNGgroupandinCgroupwereallrearedbycommondiet.TheresultsshoweddifferentdegreesofanticarcinogenicandpreventiveeffectofrefinedA.K.onMNNG-inducedlungcancersinLACAmice.A.K.notonlyexertedeffectonthenumberofinducedcancerandprecancer,causingadropofthecancerousratefrom70.87%to19.3

简介：来自哈尔滨医科大学附属第一临床医学院与上海交通大学医学院附属瑞金医学院的2个研究团队在白血病研究方面同时取得新的进展，相关成果文章分别发表在《Blood》和《CancerCell》上。

简介：Objective:Toidentifydifferentiallyexpressedlongnon-codingRNAs(lncRNAs)involvedinthemetastasisofepithelialovariancancer.Methods:AninvitroinvasionassaywasperformedtovalidatetheinvasivecapabilityofSKOV3andSKOV3.ip1celllines.TotalRNAwasthenextracted,andmicroarrayanalysiswasperformed.Moreover,ninelncRNAswereselectedforvalidationusingRT-qPCR.Results:ComparedwiththeSKOV3cells,theSKOV3.ip1cellssignificantlyimprovedintheinvitroinvasiveactivity.Ofthe4,956lncRNAsdetectedinthemicroarray,583and578lncRNAswereupregulatedanddownregulated,respectively,inSKOV3.ip1cells,comparedwiththeparentalSKOV3cells.SevenoftheanalyzedlncRNAs(MALAT1,H19,UCA1,CCAT1,LOC645249,LOC100128881,andLOC100292680)confirmedthederegulationfoundbymicroarrayanalysis.Conclusion:LncRNAsclustersweredifferentiallyexpressedinovariancancercellswithvaryingmetastaticpotentials.ThisresultindicatesthatsomelncRNAsmightexertapartialorkeyroleinepithelialovariancancermetastasis.FurtherstudiesshouldbeconductedtodeterminetherolesoftheselncRNAsinovariancancermetastasis.

简介：AbstractBackground:Previous studies have provided conflicting evidence about the increased overall survival (OS) in lung cancer patients with diabetes mellitus (DM) compared with those without DM. This study assessed progression-free survival (PFS)/OS in lung cancer patients with or without DM and tentatively analyzed the impact of blood glucose levels on PFS/OS in lung cancer patients.Methods:Data were collected from lung cancer patients based upon admission records from January 2010 to January 2012 and follow-up records from January 2010 to January 2015 in the Department of Pulmonary Medicine, Zhongshan Hospital, Fudan University, Shanghai. The data included patient sex, age, body mass index (BMI), smoking status, history of DM, level of blood glucose, pathological type, clinical stage of cancer, chemotherapy regimen, and history of anti-DM drugs. The Cox regression model and Kaplan-Meier method were used for the analysis of hazard factors and PFS/OS. For comparison of PFS/OS in lung cancer with or without DM, patients were divided into three groups: lung cancer with DM, lung cancer without DM but with elevated level of blood glucose, lung cancer without DM or elevated level of blood glucose.Results:In total, the data from 200 lung cancer patients (138 males/62 females, aged 29.0 to 78.0 years, mean 60.0 ± 8.6 years) were collected. For the comparison of PFS/OS in lung cancer patients with or without DM, patients were divided into three groups: lung cancer with DM (n = 31); lung cancer without DM but with elevated levels of blood glucose (n = 40); and lung cancer without both DM and elevated levels of blood glucose (n = 128), whereas 1 patient dropped out of the study. All the patients underwent complete chemotherapy and were followed up for 36.0 to 60.0 months. Kaplan-Meier survival analysis showed that lung cancer patients with DM had increased PFS and OS compared with those without DM (log-rank, P < 0.05, P < 0.01); the median PFS in lung cancer with DM was 12.0 months (95% confidence interval [CI], 4.0-16.0) vs. 6.0 months in those without DM (95% CI, 5.8-6.3); and the median OS in lung cancer patients with DM was 37.0 months (95% CI, 29.0-46.6) vs. 12.0 months in those without DM (95% CI, 10.9-13.1). For the other two groups of patients without DM, there was a trend toward a shorter PFS and OS in patients with elevated blood glucose compared with those without elevated blood glucose. Cox regression showed that PFS in lung cancer patients was favorably associated with the usage of anti-DM drugs, BMI, clinical stage of cancer, and chemotherapy regimen (all P < 0.05) but was inversely associated with the level of blood glucose (P < 0.05).Conclusions:Lung cancer patients with DM have prolonged PFS and OS compared with those without DM, and the level of blood glucose was inversely associated with PFS. The current results indicate that PFS may be a meaningful intermediate endpoint for OS and that the levels of blood glucose hopefully represent a prognostic factor in lung cancer patients.

简介：精子发生是取决于雄激素受体(AR)的行动的一个调整雄激素的过程。精子生产可以在为阴囊的癌症(TC)对待的人被影响，并且识别影响预定精子发生恢复追随者癌症治疗的因素是重要的。CAG和GGN重复数字影响AR的活动，这被知道；因此，如果在AR基因的CAG和GGN多型性在TC治疗以后预言精子生产的恢复，这研究的目的是调查。TC病人(n=130)在下列时间点的交付的精液：postorchiectomy并且在6，12，24，36，和60月posttherapy(T0，T6，T12，T24，T36，和T60)。CAG长度被分成三个组，<22CAG，22-23CAG，23CAG，和GGN道并且>也被分成三个组，<23GGN，23GGN，并且>23GGN。在T12，有22-23CAG的人介绍了与一统计上显著地(P=0.045)与另外的CAG比那些降低精子集中数字(8.4pp65)，基因(US28和UL96)，和在毒蛇的一个队的RNA。毒蛇的六个证实的案例被检索，修理福尔马林的嵌入石蜡的材料的完整的厚度节为anti-HMCV-IE1和anti-HCMV-pp65被染色。染色被认为积极的原子或细胞质的任何东西。DNA从50被净化。234个病人是合格的，并且(11%)25有临床上重要的流血的至少一个事件。血小板计数是吗？？

简介：AbstractBackground:Gene promoter methylation is a major epigenetic change in cancers, which plays critical roles in carcinogenesis. As a crucial regulator in the early stages of B-cell differentiation and embryonic neurodevelopment, the paired box 5 (PAX5) gene is downregulated by methylation in several kinds of tumors and the role of this downregulation in esophageal squamous cell carcinoma (ESCC) pathogenesis remains unclear.Methods:To elucidate the role of PAX5 in ESCC, eight ESCC cell lines, 51 primary ESCC tissue samples, and eight normal esophageal mucosa samples were studied and The Cancer Genome Atlas (TCGA) was queried. PAX5 expression was examined by reverse transcription-polymerase chain reaction and western blotting. Cell apoptosis, proliferation, and chemosensitivity were detected by flow cytometry, colony formation assays, and 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide assays in ESCC cell lines with PAX5 overexpression or silencing. Tumor xenograft models were established for in vivo verification.Results:PAX5 methylation was found in 37.3% (19/51) of primary ESCC samples, which was significantly associated with age (P = 0.007) and tumor-node-metastasis stage (P = 0.014). TCGA data analysis indicated that PAX5 expression was inversely correlated with promoter region methylation (r = -0.189, P = 0.011 for cg00464519 and r = -0.228, P = 0.002 for cg02538199). Restoration of PAX5 expression suppressed cell proliferation, promoted apoptosis, and inhibited tumor growth of ESCC cell lines, which was verified in xenografted mice. Ectopic PAX5 expression significantly increased p53 reporter luciferase activity and increased p53 messenger RNA and protein levels. A direct interaction of PAX5 with the p53 promoter region was confirmed by chromatin immunoprecipitation assays. Re-expression of PAX5 sensitized ESCC cell lines KYSE150 and KYSE30 to fluorouracil and docetaxel. Silencing of PAX5 induced resistance of KYSE450 cells to these drugs.Conclusions:As a tumor suppressor gene regulated by promoter region methylation in human ESCC, PAX5 inhibits proliferation, promotes apoptosis, and induces activation of p53 signaling. PAX5 may serve as a chemosensitive marker of ESCC.