OPCML基因甲基化发生率与上皮性卵巢癌发生发展的关系

卵巢癌的主要生物学特征为浸润和种植转移，最先累及盆腹腔，出现转移病灶。研究发现卵巢癌的发生和发展与表型遗传密切相关，最常见的是基因异常甲基化。甲基化调控基因表达的过程是可逆的，所以通过改变DNA甲基化状态上调肿瘤抑制基因（TSG）表达有可能成为肿瘤基因治疗的候选靶点。OPCML（opioid—binding protein／cell adhesion molecule—like）是一个鸦片受体类的细胞黏附因子，基因定位于人染色体11q25。     

熊果酸联合顺铂抑制卵巢癌生长的实验研究

目的:探讨熊果酸(UA)对卵巢癌细胞株SKOV3及卵巢癌皮下移植瘤生长的抑制作用并探讨其机制.方法:采用四甲基偶氮唑蓝(MTT)比色法,检测UA对SKOV3细胞的增殖抑制效应;建立卵巢癌皮下移植瘤模型,观察UA 对移植瘤的生长抑制作用;用免疫组化检测凋亡相关蛋白Bcl-2和Bax的表达.结果: UA对体外培养的SKOV3细胞生长具有抑制作用,与DDP联合应用使SKOV3细胞生长进一步受到抑制.体内实验表明:各治疗组肿瘤的生长明显受到抑制,而联合治疗组抗瘤作用进一步增强.UA能下调肿瘤细胞中Bcl-2蛋白的表达,同时明显提高肿瘤细胞中Bax蛋白的表达.结论:UA可明显抑制卵巢癌细胞生长,并诱导细胞凋亡,其主要机制与调节Bcl-2和Bax的蛋白表达有关.     

熊果酸联合顺铂抑制卵巢癌生长的实验研究

目的：探讨熊果酸（UA）对卵巢癌细胞株SKOV3及卵巢癌皮下移植瘤生长的抑制作用并探讨其机制。方法：采用四甲基偶氮唑蓝（MTT）比色法,检测UA对SKOV3细胞的增殖抑制效应;建立卵巢癌皮下移植瘤模型,观察UA对移植瘤的生长抑制作用;用免疫组化检测凋亡相关蛋白Bcl-2和Bax的表达。结果：UA对体外培养的SKOV3细胞生长具有抑制作用,与DDP联合应用使SKOV3细胞生长进一步受到抑制。体内实验表明：各治疗组肿瘤的生长明显受到抑制,而联合治疗组抗瘤作用进一步增强。UA能下调肿瘤细胞中Bcl-2蛋白的表达,同时明显提高肿瘤细胞中Bax蛋白的表达。结论：UA可明显抑制卵巢癌细胞生长,并诱导细胞凋亡,其主要机制与调节Bcl-2和Bax的蛋白表达有关。     

c-myc和K-ras对小鼠卵巢上皮细胞体外转化和体内致瘤的研究

目的探讨癌基因c-myc和K-ras在卵巢癌发生发展中的作用。方法用逆转录病毒转基因系统,将正常的c-myc基因和突变的K-ras基因先后导入小鼠卵巢上皮（MOSE）细胞,建立表达c-myc和K-ras基因的细胞株,分别称为MOSE-Myc细胞、MOSE-Ras细胞和MOSE-RM细胞。通过细胞增殖实验、克隆形成实验、体外侵袭实验以及体内成瘤实验,研究转基因后MOSE细胞生物学特性的改变及恶性转化。结果c-myc和K-ras基因容易被重组逆转录病毒导入MOSE细胞,转导后靶细胞内分别有相应的c-myc或K-ras mRNA转录,以及相应的c-myc（62ooo）和K-ras（21000）蛋白的表达。MOSE-Ras组和MOSE-RM（MOSE-Ras／Myc）组细胞增殖能力显著强于MOSE和MOSE-Myc组（P〈0．01）,MOSE-RM组细胞增殖能力显著强于MOSE-Myc组（P〈0．05）。MOSE-Ras和MOSE-RM组在软琼脂培养中均能形成克隆集落,而MOSE组和MOSE-Myc组不能形成克隆集落。MOSE-Ras组和MOSE-RM组能够穿透Matrigel,具有侵袭能力。MOSE-Ras组和MOSE-RM组细胞在裸鼠体内形成肿瘤,且肿瘤组织细胞仍然可见有K-ras和c-myc蛋白的表达;而MOSE组和MOSE-Myc组无肿瘤形成。结论重组逆转录病毒载体作为转基因的工具,转导效率高,可稳定表达,可以感染正常的细胞;突变的K-ras可使MOSE发生恶性转化,在体内形成肿瘤;c-myc作为一个核转录调节因子,不能使MOSE发生恶性转化,但可协同其他因子,加强其他因子的功能。     

人卵巢癌裸鼠移植瘤模型的建立及其生物学特性的实验应用研究

研究用1例人卵巢癌淋巴转移的癌组织直接移植于裸鼠皮下,建成一株人卵巢癌移植瘤动物模型,已传至第26代.移植成功率达100%,平均裸鼠带瘤存活中位数为102天.肿瘤倍增时间为7.17(SD=±1.02天).组织学和超微结构形态证实保持了原人肿瘤的特征,有淋巴结转移行为.人类肿瘤染色体特征.保留了分泌癌胚抗原的能力.具有P53癌基因蛋白的异常表达.移植瘤细胞可在体外培养并传至5代.流式细胞仪及显微分光光度计检测移植瘤,提示肿瘤为多倍体,各代移植瘤的DNA指数与第一代肿瘤基本一致(DI1.05~1.40).经初步应用研究,用传代移植瘤组织提取抗原免疫BALB/C小鼠,将免疫小鼠的脾细胞与小鼠缺欠型骨髓瘤系进行融合,制备了一株抗卵巢癌单克隆抗体,经免疫组化染色(ABC法)可显示有与人卵巢癌阳性反应.说明裸鼠人体卵巢癌模型的建立,为深入进行该类肿瘤诊断及治疗研究提供了有效途径.     

卵巢癌特异性免疫细胞治疗的体内外实验研究

背景与目的:卵巢癌抗独特型微抗体(6B11mini)是部分人源化的抗独特型卵巢癌疫苗,体内外实验研究证明,它可以诱导出特异的抗卵巢癌体液免疫和细胞免疫.本研究评价将6B11mini作为抗原,采用免疫细胞的方法处理卵巢癌时的安全性和有效性.方法:用纯化的6B11mini负载树突细胞(dendritic cell,DC),与外周血单个核细胞(peripheral blood mononucleocyte,PBMNC)混合培养,在多种细胞因子共同作用下获得效应细胞6B11-OCIK.通过软琼脂克隆形成实验及接种裸鼠皮下瘤实验,观察6B11-OCIK在体内和体外的成瘤能力;将6B11-OCIK静脉注射BALB/c小鼠,观察急性毒性反应:体外51Cr释放实验检测6B11-OCIK对靶细胞的杀伤作用.用人卵巢癌细胞株SKOV3构建严重联合免疫缺陷(severe combined immune deficieney,SCID)小鼠卵巢癌移植瘤模型,注射6B11-OCIK,并以CIK、PBMNC细胞以及生理盐水作为对照组,分别观察各组肿瘤生长情况.结果:软琼脂培养14 d,卵巢癌SKOV3细胞克隆形成良好,克隆形成率50%:皮下接种裸鼠后14 d,阳性对照的宫颈癌HeLa细胞组全部成瘤,6B11-OCIK、CIK、WI-38组和新鲜PBMNC组持续观察13周没有成瘤.6B11-OCIK静脉注射BALB/c小鼠,30 min内各剂量实验组和生理盐水对照组动物都无任何明显的不良反应:输注后第13天处死小鼠,解剖小鼠观察其各主要脏器无明显异常.在体外杀伤实验中6B11-OCIK对抗原阳性的肿瘤细胞具有特异性杀伤作用,并且与MHC限制性相关;在荷瘤SCID小鼠中6B11-OCIK治疗组肿瘤重量与生理盐水对照组相比差异有统计学意义(P=0.023),与CIK组、新鲜单采组相比差异无统计学意义(P=0.540,P=0.285).结论:6B11-OCIK在动物体内应用时符合安全性指标,并对卵巢癌的生长有一定的抑制作用.     

卵巢癌高频转移细胞模型中nm23-H1基因表达的相关性研究

目的 筛选高频转移卵巢恶性肿瘤细胞，研究不同转移潜能的细胞和nm23的相关性。方法 通过反复动物接种和体外培养，观察动物肺转移状况，筛选高频转移细胞株，比较原发肿瘤和转移肿瘤的特征，并应用Northera-blot方法测定各类肿瘤细胞nm23 mRNA表达水平。结果 8株卵巢恶性肿瘤细胞中4株有较高转移潜能。多次培养接种可筛选出高频转移细胞亚群。测定各类细胞nm23 mRNA表达水平与肿瘤转移特性呈负相关。结论 由基因分子水平决定的肿瘤转移趋势在不同肿瘤种类及细胞亚群中有明显差异；卵巢癌中nm23 mRNA和蛋白的表达与其转移能力的降低有密切关系，可作为判定卵巢癌预后的敏感指标。     

RhoA基因沉默抑制卵巢癌腹腔移植瘤恶性生物学行为的研究

目的:研究慢病毒介导RhoA基因沉默对人卵巢癌裸鼠腹腔移植瘤生长、侵袭及转移等恶性生物学行为的影响。方法:21只裸鼠随机分为HO8910-RhoA-shRNA组、HO8910-RhoA-NC组和HO8910组,每组7只。细胞接种法建立人卵巢癌腹腔移植瘤模型,每2天测量腹围。4周后解剖裸鼠,大体观察,测定腹水量,统计肿瘤播散器官数及瘤结节数。称量瘤体重量,并计算抑瘤率。镜下观察,应用HE染色分析移植瘤病理形态学特点。实时荧光定量PCR和Western blot检测移植瘤RhoA mRNA和蛋白表达情况。TUNEL技术检测移植瘤凋亡指数(apoptotic index,AI)。结果:与HO8910-RhoA-NC组和HO8910组比较,HO8910-RhoA-shRNA组裸鼠腹围增长明显滞后(P<0.05),腹水量明显减少(P=0.01),肿瘤播散器官数、瘤结节数及瘤体重量均明显减少(P均<0.001),抑瘤率达70.62%。RhoA基因mRNA和蛋白表达水平均显著下降(P均<0.001)。凋亡指数AI明显升高(P<0.001)。结论:慢病毒靶向沉默RhoA基因能显著抑制人卵巢癌裸鼠腹腔移植瘤的恶性生物学行为。     

环状RNA hsa-circ-0006361对卵巢癌SKOV3细胞小鼠移植瘤生长的影响

目的:基于前期RNA-seq测序发现hsa-circ-0006361在卵巢癌中高表达,为研究hsa-circ-0006361在上皮性卵巢癌发生发展中的作用,我们研究了hsa-circ-0006361对人上皮性卵巢癌裸鼠移植瘤生长、裸鼠生存时间的影响.方法:分离细胞核与细胞质后分别提取RNA进行RT-qPCR及琼脂糖凝胶...     

HMGA1基因小分子RNAi对卵巢癌转移抑制的实验研究

目的：探讨高迁移率蛋白家族A1（high mobility group A1,HMGA1）基因小分子干扰RNA对卵巢癌转移抑制的机理。方法：RT—PCR一步法检测3种不同的卵巢癌细胞株中HMGA1、E钙黏蛋白mRNA的表达水平;设计并合成HMGA1 siRNA,转染H08910PM细胞：半定量RT—PCR分析法观察HMGA1 siRNA转染对E钙黏蛋白mRNA表达的逆转作用,及对卵巢癌细胞株体外侵袭、运动的抑制作用。结果：RT—PCR半定量分析结果显示：OVCAR-3细胞中HMGA1 mRNA表达量相对较低（0．64±0．13）,而E-钙黏蛋白mRNA仅在OVCAR-3细胞中有表达;H08910PM细胞稳定转染HMGA1 siRNA后,转染组、对照组HMGA1 mRNA表达水平分别为0．16±0．08、0．47±0．11（P〈0．01）,E钙黏蛋白mRNA表达水平分别为0．38±0．07、0．09±0.05（P〈0．01）;体外运动实验显示,跨膜细胞数转染组明显低于对照组（P〈0．05）;重组细胞基底膜侵袭实验显示,穿透基底膜细胞数转染组明显低于对照组（P〈0．01）。结论：HMGA1基因与卵巢癌转移密切相关,HMGA1基因siRNA可上调卵巢癌细胞中E钙黏蛋白的表达,抑制卵巢癌细胞的运动和侵袭,为卵巢癌转移的基因治疗提供新的靶点。     

罗格列酮促进卵巢癌细胞凋亡的体内实验研究

[目的]探讨过氧化物酶体增殖物激活受体γ（PPAR-γ）配体罗格列酮（RGZ）对人卵巢浆液性乳头状囊腺癌SKOV3细胞的抑制作用。[方法]建立卵巢癌SKOV3细胞裸鼠移植瘤模型,观察不同剂量RGZ对移植瘤体积的影响;HE染色观察各组移植瘤组织细胞形态学变化;免疫细胞化学法观察移植瘤中Bcl-2、Cytochrome C蛋白表达水平。[结果]RGZ组（4mg/kg,12mg/kg,60mg/kg,120mg/kg）裸鼠移植瘤体积分别为0.190±0.023mm3、0.065±0.003mm3、0.195±0.004mm3和0.182±0.023mm3,较对照组（0.300±0.016mm3）均明显缩小,差异有统计学意义（P〈0.05）。抑瘤率分别为36.7%、78.3%、35.0%和40.0%。HE染色观察RGZ作用SKOV3细胞后有变性细胞、单细胞死亡及大面积的凝固性坏死。Bcl-2在RGZ组（60mg/kg,120mg/kg）中的表达较对照组显著下调,Cytochrome C在RGZ组（60mg/kg,120mg/kg）中的表达较对照组显著上调,差异均有统计学意义（P〈0.05）。[结论]RGZ对卵巢癌裸鼠移植瘤有明显抑制作用,可促进凋亡。提示PPAR-γ可能成为卵巢癌治疗的新分子靶点。     

Anti-proliferation Effects of Isorhamnetin on Lung Cancer Cells in Vitro and in Vivo

Background: Isorhamnetin (Iso), a novel and essential monomer derived from total flavones of Hippophaerhamnoides that has long been used as a traditional Chinese medicine for angina pectoris and acute myocardialinfarction, has also shown a spectrum of antitumor activity. However, little is known about the mechanisms ofaction Iso on cancer cells. Objectives: To investigate the effects of Iso on A549 lung cancer cells and underlyingmechanisms. Materials and Methods: A549 cells were treated with 10~320 μg/ml Iso. Their morphological andcellular characteristics were assessed by light and electronic microscopy. Growth inhibition was analyzed byMTT, clonogenic and growth curve assays. Apoptotic characteristics of cells were determined by flow cytometry(FCM), DNA fragmentation, single cell gel electrophoresis (comet) assay, immunocytochemistry and terminaldeoxynucleotidyl transferase nick end labeling (TUNEL) . Tumor models were setup by transplanting Lewislung carcinoma cells into C57BL/6 mice, and the weights and sizes of tumors were measured. Results: Isomarkedly inhibited the growth of A549 cells with induction of apoptotic changes. Iso at 20 μg/ml, could induceA549 cell apoptosis, up-regulate the expression of apoptosis genes Bax, Caspase-3 and P53, and down-regulatethe expression of Bcl-2, cyclinD1 and PCNA protein. The tumors in tumor-bearing mice treated with Iso weresignificantly smaller than in the control group. The results of apoptosis-related genes, PCNA, cyclinD1 and otherprotein expression levels of transplanted Lewis cells were the same as those of A549 cells in vitro. Conclusions:Iso, a natural single compound isolated from total flavones, has antiproliferative activity against lung cancer invitro and in vivo. Its mechanisms of action may involve apoptosis of cells induced by down-regulation of oncogenesand up-regulation of apoptotic genes.     

OPCML is frequently methylated in human colorectal cancer and its restored expression reverses EMT via downregulation of smad signaling

Emerging evidence has indicated that the expression of OPCML gene is frequently altered in a variety of cancers. We previously demonstrated that the OPCML gene is a target of epigenetic inactivation and its gene product exhibits tumor-suppressive properties. However, little is known regarding the effects and mechanisms of OPCML in colon cancer. We show that the loss or downregulation of OPCML is associated with its promoter hypermethylation. Methylation of the OPCML promoter was detected in all tumors and tumor-adjacent tissues, but lower methylation in normal colon tissues. The drug-induced release of epigenetic silencing was able to restore OPCML expression and the re-expression led to the suppression of cell growth. Furthermore, the increase in OPCML expression reversed a partial epithelial-to-mesenchymal (EMT)-like transition. Cell migration and invasiveness were also inhibited in response to OPCML upregulation. These actions were mediated through the inactivation of TGFβ-Smad signaling pathways. In addition, OPCML expression was associated with two upstream nuclear receptors (ERRa and RORa). Altogether, our study reveals OPCML as a potential tumor suppressor gene epigenetically silenced in colon cancer. Our study will help to elucidate the anti-invasive mechanisms of OPCML and establish new chemotherapeutic strategies for human colon cancer.     

Suppression of Metastatic Murine Ovarian Cancer Cells by Transduced Embryonic Progenitor Cells

Ovarian cancer is the leading cause of death among gynecological malignancies. Chemotherapy alone is not sufficient to achieve long-term survival of the patient with advanced stage ovarian cancer. Although cancer immune therapy has long been expected as a new modality for ovarian cancer, very few trials have been clinically successful. One of the reasons for the failure in practical immune therapy is the immune-suppressive cancer microenvironment. We have reported that immune-suppressive molecules including PD-L1, Cox or ULBP-2 are expressed in human ovarian cancer, and they suppress local tumor immunity by disturbing CD8+T cell infiltration. Thus, we attempted to develop an immune therapy that can target multiple metastatic foci and increase CD8+T cell infiltration by altering local tumor environment. Endothelial progenitor cells (EPC) were transduced with the chemokine CCL19. When injected intravenously, this "immune-stimulatory EPC" was incorporated efficiently into local tumor vessels, and exerted an anti-tumor effect in a subcutaneous tumor model, a lung metastasis model and a peritoneal dissemination model. The anti-tumor effect was not observed when immunodeficient mice were used for the experiment, suggesting that the effect is mediated by immune cells. These results suggest that EPC are ideal carriers with which to deliver immune-stimulatory signals to multiple remote metastases. Alteration of local immune environment by this method may be used in the future for individualized cancer immune therapy.     

细胞凋亡检测用于卵巢癌实体瘤体外化疗药物敏感试验

目的 评价细胞凋亡检测用于实体瘤体外化疗药物敏感试验的可行性。方法 对Ⅲｃ期原发性上皮性卵巢癌实体瘤细胞行体外分离培养,使用６种不同的抗肿瘤药物对其进行处理,经５天培养后,制成细胞涂片,末端标记法观察不同药物作用后细胞凋亡情况。结果 发现源一示同病例的卵巢癌实体瘤细胞对不同抗癌药物的敏感性存在差异,同一种抗癌药物对不同病人卵巢癌实体瘤细胞产生的凋亡程度不同。结论 细胞凋亡检测用于肿瘤的药物敏感试验     

CpG岛甲基化表型及OPCML基因甲基化与肝细胞癌发生的关系

背景与目的：CpG岛甲基化表型（CpG island methylator phenotype,CIMP）涉及到多个基因启动子同时甲基化,具有肿瘤特异性,与多种肿瘤的发生或预后相关。但有关肝癌CPG岛甲基化表型的研究罕见报道。OPCML（opioid-binding protein／cell adhesion molecule—like）基因目前多为针对上皮性卵巢癌的研究．被认为是卵巢癌的候选抑癌基因。本研究旨在探讨CIMP及OPCML基因与肝癌的发生是否有关。方法：运用甲基化特异性PCR方法检测50例肝细胞癌组织及48例癌旁组织中OPCML、p15、SOCS-1、GST-P、RAR．b、p16、p73、p14、MGMT和hMLHl基因的甲基化状况。结果：肝癌组织甲基化率普遍比相应癌旁组织甲基化率高：OPCML（70．0％VS．64．6％）、p15（58．0％VS．50．0％）、SOCS-1（78．0％VS．50．0％）、GST—P（56．0％VS．27．1％）、RAR-b（30．0％vs．6．3％）、p16（26．0％vs．14．6％）、p73（16．0％vs．0％）、p14（36．0％vs．27．1％）、MGMT（16．0％vs．10．4％）和hMLH1（18．O％VS．4．2％）。SOCS-1,GST-p,RAR-b,p16和p73基因甲基化率在肝癌组与癌旁组差异有显著性（P〈0．05）,其它基因两组之间的甲基化率差异无显著性。CIMP阳性组（同时具有≥3个位点甲基化）复发时间较早,1年无瘤生存率为18．2％,而CIMP阴性组（具有〈3个位点甲基化）复发时间较晚,1年无瘤生存率为75．0％（P〈0．05）。结论：肝癌中存在着CpG岛甲基化表型（CIMP）。CIMP可作为肝癌患者预后判断的指标之一：OPCML基因甲基化可能在肝癌的发生中发挥重要的作用。     

Effects of Valproic Acid on Proliferation,Apoptosis, Angiogenesis and Metastasis of Ovarian Cancer in Vitro and in Vivo

Inhibitors of histone deacetylase activity are emerging as a potentially important new class of anticanceragents. In this study, we assessed the anticancer effects of valproic acid (VPA) on ovarian cancer in vitro and invivo. Cultured SKOV3 cells were treated by VPA with different concentrations and time, then the effects on cellgrowth, cell cycle, apoptosis, and related events were investigated. A human ovarian cancer model transplantedsubcutaneously in nude mice was established, and the efficacy of VPA used alone and in combination withdiammine dichloroplatinum (DDP) to inhibit the growth of tumors was also assessed. Proliferation of SKOV3 cellswas inhibited by VPA in a dose and time dependent fashion. The cell cycle distribution changed one treatmentwith VPA, with decrease in the number of S-phase cells and increase in G1-phase. VPA could significantly inhibitthe growth of the epithelial ovarian cancer SKOV3 cells in vivo without toxic side effects. Treatment with VPAcombined with DDP demonstrated enhanced anticancer effects. The result of flow cytometry (FCM) indicatedthat after VPA in vitro and in vivo, the expression of E-cadherin was increased whereas vascular endothelialgrowth factor (VEGF) and matrix metalloproteinase-9 (MMP-9) were decreased. This study suggests that VPAcould be a novel attractive agent for treatment of ovarian cancer.     

脐血来源树突状细胞体外诱导抗卵巢癌免疫特异性

[目的]研究脐血来源树突状细胞(DC)体外诱导特异性抗卵巢癌细胞的免疫效应.[方法]①从脐血中分离单个核细胞(MNCs)后,获得单核细胞(Mo).粒单集落刺激因子(GM-CSF)和白介素4(IL-4)诱导分化,培养7天后应用流式细胞仪进行细胞表型分析.②诱导单核细胞分化的第3天加入人卵巢癌细胞株3AO的冻融抗原,共培养4天后获得负载肿瘤抗原的成熟DC;将致敏DC与从脐血中分离的同种异体T淋巴细胞共培养3天,获得细胞毒T淋巴细胞(CTL);四甲基偶氮唑蓝(MTT)法检测CTL及上清对人卵巢癌细胞株3AO、人胚肾细胞株293T(对照细胞)、人肝癌细胞株HCCC-9810的细胞毒作用.[结果]①脐血来源单核细胞(Mo)在GM-CSF和IL-4作用下,7天后可分化生成成熟的DC,高表达DC特异性抗原CDla、CD80(B7-1)、CD86(B7-2)、HLA-DR、CD83.②DC可负载并递呈肿瘤抗原,激活同种异体T淋巴细胞,诱导肿瘤特异性CTL产生.不同浓度CTL及上清对卵巢癌细胞3AO有特异性杀伤、抑制作用(P＜0.05).[结论]脐血中单核细胞可体外分化扩增为成熟的功能性DC,并诱导出特异性杀伤卵巢癌细胞的免疫效应.     

卵巢癌细胞和脐血树突状细胞融合瘤苗抗肿瘤免疫效应的初步研究

目的：将脐血来源的树突状细胞（DC）与人卵巢癌细胞株SKOV3细胞相融合，获得SKOV3/DC融合细胞，分析其生物学特性及体外诱导抗卵巢癌肿瘤免疫的能力.方法：1）将用PKH26红色荧光染料标记脐血来源的DC后，聚乙二醇法（PEG）融合DC与人卵巢癌细胞株SKOV3细胞，流式细胞仪分选融合细胞.2）应用细胞培养技术、流式细胞术及光学显微镜检测SKOV3/DC的生长特性和形态学特征 四甲基偶氮唑蓝（MTT）法观察融合细胞体外刺激混合淋巴细胞反应的能力及诱导特异性肿瘤免疫的能力.结果：1）DC和SKOV3按10∶1比例融合，融合率约为8.5%.融合细胞可在体外缓慢增殖，CA125抗原及CD1a、CD80、CD86、HLA-DR、MHC-Ⅰ分子表达阳性.2）SKOV3/DC在体外能有效的激发混合淋巴细胞增殖反应，可明显激活细胞毒性T淋巴细胞（CTL），对卵巢癌细胞株SKOV3有特异性杀伤效应.结论：利用PEG法制备的SKOV3/DC融合细胞兼具两种亲本细胞的部分特性，在体外能够诱导特异性抗肿瘤免疫.本研究将SKOV3/DC作为肿瘤疫苗，为其在卵巢癌主动免疫治疗研究中的进一步应用打下了基础.