NFATc1对裸鼠上皮性卵巢癌移植瘤脉管生成的影响

 目的: 探讨胞浆活化T细胞核因子1(nuclear factor of activated T-cells, cytplasmic 1, NFATc1)对人卵巢癌SKOV3细胞裸鼠移植瘤生长和肿瘤脉管生成的影响及其可能机制。方法: NFATc1 siRNA转染人上皮性卵巢癌细胞株SKOV3,免疫荧光及RT-PCR测量转染效率和基因抑制率,选取效率最高的序列建立裸鼠皮下移植瘤模型, 测量各组裸鼠肿瘤体积,观察NFATc1 siRNA的体内抗肿瘤作用。免疫组织化学检测各组肿瘤组织NFATc1的表达情况,并使用细胞角蛋白染色标记上皮性来源,CD34标记微血管,podoplanin标记微淋巴管。分别计算各组微血管及微淋巴管密度并进行统计学分析。应用RT-PCR及Western blot检测各组移植瘤组织NFATc1、CXC趋化因子受体2(CXCR2)、成纤维细胞生长因子2(FGF-2)及血小板源性生长因子BB(PDGF-BB)的mRNA及蛋白表达水平。结果: 3条特异性序列均可显著降低NFATc1的表达水平,以siRNA-1169最佳。NFATc1在空白组及阴性对照组瘤组织高表达。干扰组抑瘤率为57.08%,且重量和体积均低于2个对照组。空白组和阴性对照组的微血管密度和微淋巴管密度明显高于干扰组。对照组比较,NFATc1 siRNA可以在mRNA水平上明显抑制NFATC1、CXCR2、FGF-2和PDGF-BB的转录。Western blot各组细胞在相应位置出现NFATc1、CXCR2、FGF-2和 PDGF-BB条带,空白组与阴性对照组的吸光度最强,与干扰组比较具有显著差异。结论: NFATc1 siRNA明显抑制人卵巢癌SKOV3细胞裸鼠皮下移植瘤生长和肿瘤脉管生成,下调CXCR2、FGF-2及PDGF-BB的表达可能为其途径之一。     

碱性成纤维细胞生长因子与卵巢癌的关系

目的　探讨碱性成纤维细胞生长因子 (basic fibroblast growth factor,b FGF)对卵巢癌细胞增殖、浸润和肿瘤血管生成的影响 ,及 b FGF单克隆抗体 (b FGF monoclonal antibody,b FGF- MAb)的治疗作用。　方法　将人卵巢癌细胞株 SKOV3接种于 2 4孔板 ,加入不同浓度的 b FGF,每日行结晶紫染色后测定光密度 (D4 90 )值 ,绘制细胞生长曲线 ;将 SKOV3细胞团接种于铺设有细胞外基质凝胶的 4孔板 ,每日测定癌细胞在凝胶中的浸润距离 ;建立 SKOV3细胞裸鼠皮下移植瘤模型 ,每周两次分别将 b FGF、b FGF-MAb和生理盐水注射于移植瘤周围 ,8周后测量肿瘤体积 ;对移植瘤组织切片行 因子的免疫组化染色、测定肿瘤内微血管密度 (microvessel density,MVD)。　结果　 b FGF能促进 SKOV3细胞增殖并呈浓度依赖 ,实验第 5天 ,5 ng/ml、10 ng/ml组细胞 D4 90 值是对照组的 1.0 9倍和 1.2 1倍 ;b FGF能促进 SKOV3细胞浸润并呈浓度依赖 (P<0 .0 5 ) ,第 7天 ,5 ng/ml、10 ng/ml组细胞浸润距离分别是对照组的 1.5 3倍和2 .4 5倍 ;b FGF组移植瘤体积和 MVD分别是对照组的 1.80倍和 1.4 6倍 (P<0 .0 5 ) ,b FGF- MAb组移植瘤体积和 MVD分别是对照组的 6 3.7%和 6 2 .8% (P<0 .0 5 )。　结论　b FGF能明显促进卵巢癌细胞的增殖、     

建立卵泡刺激素受体单位点基因突变体的卵巢癌SKOV3细胞和裸鼠模型

目的 建立转染卵泡刺激素受体（FSHR）307和680位点突变的上皮性卵巢癌SKOV3细胞系和裸鼠动物模型。方法 将人卵巢颗粒细胞（来自体外受精取卵时废弃的颗粒细胞）,行原代培养后用于FSHR RNA提取;FSHR和FSHR307、680位点突变重组蛋白构建;将FSHR和FSHR307、680位点突变蛋白转染SKOV3细胞株;将处理后的3组SKOV3细胞接种到裸鼠皮下,8周后处死裸鼠,并取瘤组织验证。     

CD44和NANOG在上皮性卵巢癌中的表达及其临床意义

目的:探讨上皮性卵巢癌(epithelial ovarian cancer,EOC)中CD44及转录因子NANOG的表达及其临床意义。方法:用免疫组织化学法检测良性卵巢肿瘤和EOC组织中CD44及NANOG的表达,并对EOC中CD44和NANOG的表达水平做相关性分析。Western blot法检测不同浓度顺铂对卵巢癌SKOV3细胞中CD44及NANOG蛋白表达水平的影响。结果:CD44和NANOG在EOC中的阳性表达率均明显高于良性卵巢肿瘤组织(P0.01);EOC中CD44与NANOG的表达水平呈正相关(r=0.346,P0.01)。CD44在EOC中的阳性表达率与临床分期和淋巴结转移有关(P0.05),而与年龄、病理分级、病理类型和肿瘤位置无关;NANOG在EOC中的阳性表达率与病理分级和临床分期有关(P0.05),而与年龄、病理类型、淋巴结转移和肿瘤位置无关。顺铂可诱导卵巢癌SKOV3细胞中CD44和NANOG表达上调(P0.05)。结论:CD44和NANOG在EOC中高表达,且与EOC发生和发展有关。顺铂可诱导卵巢癌SKOV3细胞中肿瘤干细胞标记物CD44及胚胎干细胞多能性基因产物NANOG表达升高。肿瘤干细胞的产生可能是促进EOC发生、发展及化疗耐药的潜在机制。     

CD44 and β1 Integrin Mediate Ovarian Carcinoma Cell Adhesion to Peritoneal Mesothelial Cells

Epithelial cancer of the ovary spreads by implantation of tumor cells onto the mesothelial cells lining the peritoneal cavity. The aim of this study was to identify the adhesion molecules involved in the interaction of ovarian carcinoma cells with mesothelial cells. The human ovarian carcinoma cell lines SKOV3 and NIH:OVCAR5 as well as LP9 cells, a human peritoneal mesothelial cell line, were analyzed by flow cytometry for the expression of CD44 and the beta1 integrin subunit. An in vitro adhesion assay was developed whereby LP9 cells were grown as confluent monolayers, and radiolabeled ovarian carcinoma cells were monitored for their ability to adhere to the mesothelial monolayer in the presence of potential inhibitors. Each cell line was evaluated for the presence of a pericellular matrix by a particle exclusion assay. A monoclonal antibody (MAb) against the beta1 integrin subunit significantly reduced the adhesion of SKOV3 cells to LP9 cells, whereas NIH:OVCAR5 adhesion to LP9 cells was significantly inhibited by a CD44 MAb. The LP9 cells produced both hyaluronic acid (a ligand for CD44) as well as several extracellular matrix molecules (ligands for the beta1 integrin heterodimers). These results suggest that both CD44 and the beta1 integrin heterodimers may play a role in mediating the adhesion of ovarian carcinoma cells to mesothelial cells.     

抗HER-2工程抗体chA21对人卵巢癌SKOV3裸小鼠移植瘤血管生成的影响

目的 探讨抗HER-2工程抗体chA21对过表达HER-2的人卵巢癌细胞株SKOV3裸小鼠移植瘤血管生成的影响.方法 建立人卵巢癌SKOV3裸小鼠移植瘤模型,随机分成阴性对照组和chA21组,连续5周尾静脉注射给药,观察肿瘤生长变化;5周后处死裸鼠取下瘤体,利用组织芯片及免疫组化方法结合显微图像分析系统定量检测VEGF、DLL4表达情况,并用CD31免疫组化染色比较两组微血管密度(MVD)值.结果 chA21组肿瘤组织中VEGF、DLL4的表达及MVD值均显著低于阴性对照组(P<0.05).结论 抗HER-2工程抗体chA21能显著抑制人卵巢癌SKOV3裸小鼠移植瘤的血管生成.     

靶向上皮性卵巢癌SKOV3细胞ZEB1-shRNA重组体构建及功能研究

目的:利用RNA干扰技术,降低人上皮性卵巢癌SKOV3细胞中锌指增强子结合蛋白1(ZEB1)基因的表达,观察ZEB1低表达对SKOV3细胞的生长影响。方法:用pSUPER-EGFP1载体构建针对人ZEB1基因的干扰质粒shZEB1,脂质体转染SKOV3细胞,G418筛选稳定转染细胞株,通过RT-PCR和Western blot检测ZEB1在SKOV3细胞中表达。用克隆形成、划痕试验、RT-PCR和致瘤试验分别检测转染细胞克隆能力、迁移力、miR-200c表达水平和在裸鼠的致瘤性。结果:成功构建shZEB1,稳定转染细胞株shZEB1-SKOV3内ZEB1表达下降,导致shZEB1-SKOV3细胞miR-200c表达增高,克隆能力、迁移力及致瘤性下降。结论:用RNA干扰技术可靶向降低卵巢癌细胞株SKOV3内ZEB1的表达,使其致瘤性降低,提示ZEB1可作为分子靶点用于上皮性卵巢癌靶向治疗。     

小干扰RNA抑制卵巢癌模型裸鼠移植瘤葡萄糖调节蛋白94的表达及意义

背景：一些实验在模型鼠移植瘤中葡萄糖调节蛋白94被敲除后,细胞黏附中断,刺激肝起源细胞增殖,进而促进肝肿瘤的发生,推测葡萄糖调节蛋白94在肝癌中起到保护作用。 目的：应用小干扰RNA技术抑制裸鼠卵巢癌模型皮下移植瘤内质网分子伴侣葡萄糖调节蛋白94的基因表达,探讨移植瘤中葡萄糖调节蛋白94基因及蛋白表达的变化对移植瘤生长的影响。 方法：从GeneBank中选取人类葡萄糖调节蛋白94基因序列,构建受控于人RNA聚合酶Ⅲ启动子U6 的真核表达载体psiSTRIKETM/葡萄糖调节蛋白94。建立人卵巢癌HO-8910细胞株裸鼠皮下接种模型,并将真核表达载体转染入裸鼠移植瘤体内,观察肿瘤生长情况。卵巢癌裸鼠模型经过不同给药方案干预后分为特异性小干扰RNA组,非特异性小干扰RNA组和生理盐水对照组, RT-PCR和免疫组化SP法检测葡萄糖调节蛋白94 mRNA和蛋白在肿瘤内的表达情况,并观察模型裸鼠的移植瘤生长情况。 结果与结论：成功构建RNA干扰质粒载体,所有裸鼠模型均接种成功,5 d后即可见皮下肿瘤形成,14 d左右肿瘤直径达7-10 mm。转染质粒完毕后抑瘤率为65.1%,与非特异性小干扰RNA组和生理盐水对照组比较,差异有显著性意义(P < 0.01)。psiSTRIKETM/GRP94治疗后瘤体内葡萄糖调节蛋白94 mRNA和蛋白显著下调(P < 0.01)。说明靶向葡萄糖调节蛋白94 mRNA的小干扰RNA可显著抑制人卵巢癌裸鼠移植瘤的生长,其机制可能是诱导葡萄糖调节蛋白94 mRNA和蛋白表达下调所致。 中国组织工程研究杂志出版内容重点：肾移植;肝移植;移植;心脏移植;组织移植;皮肤移植;皮瓣移植;血管移植;器官移植;组织工程全文链接：     

Down-regulation of UTP23 promotes paclitaxel resistance and predicts poorer prognosis in ovarian cancer

ObjectiveFrequent resistance to paclitaxel and carboplatin based chemotherapy remains a therapeutic challenge in ovarian cancer. UTP23, a small sub-unit processome component, is down-regulated in a paclitaxel-resistant cell line SKOV3-TR30 compared with its parental SKOV3 cells based on our previous study. However, the specific mechanism of UTP23 in regulating ovarian cancer chemotherapy resistance remains largely unknown.MethodsImmunohistochemical (IHC) staining was used to measure UTP23 expression in 133 ovarian cancer tissues. Then we used short hairpin RNA (shRNA), over-expression plasmid and cell counting kit-8 (CCK-8) assay to evaluate the function of UTP23 on modulating paclitaxel resistance in ovarian cancer. RNA-sequencing (RNA-seq) was used to find targeted downstream molecular of UTP23. Quantitative real-time polymerase chain reaction (qRT-PCR) and western blotting were utilized to detect related genes expression.ResultsWe confirmed that UTP23 was down-regulated in both SKOV3-TR30 and A2780-TR cells compared with their parental cells. Decreased UTP23 expression was observed in ovarian cancer tissues with paclitaxel resistance. Moreover, lower expression of UTP23 was tightly correlated with patients of worse prognosis. Further UTP23 silence by shRNA increased paclitaxel resistance in SKOV3 and A2780 cells. And UTP23 over-expression by plasmid decreased paclitaxel resistance in SKOV3-TR30 and A2780-TR cells. Additionally, RNA-seq and qRT-PCR validation revealed that growth differentiation factor 15 (GDF15) was probably a downstream target for UTP23. GDF15 was notably up-regulated upon the depletion of UTP23 in both SKOV3 and A2780 cells.ConclusionOur findings elucidated a previously unknown function for UTP23 in regulating paclitaxel sensitivity and UTP23 could serve as a potential prognostic predictor for ovarian cancer.     

JAK2,HSP基因蛋白表达与卵巢癌紫杉醇化疗耐药相关性的研究

目的检测卵巢癌细胞株及紫杉醇化疗后卵巢癌组织中JAK2,HSP,基因蛋白表达的变化,探讨其与卵巢癌紫杉醇化疗耐药的关系及临床意义。方法选用卵巢癌紫杉醇耐药细胞株SKOV3/TAX及敏感细胞株SKOV3,及58例卵巢癌组织,包括卵巢癌术后及紫杉醇化疗后复发患者19例（化疗组）,术前未化疗患者39例（未化疗组）。采用免疫组化二步法,检测卵巢癌组织及细胞中JAK2,HSP基因的蛋白表达。结果 1.光镜下观察SKOV3/TAX细胞株中JAK2、HSP蛋白表达强度均明显高于SKOV3细胞株;组织中化疗组与未化疗组相比JAK2,HSP的蛋白表达累积光密度值均明显增加（分别为：36987.38±16873.42 vs 27756.29±7136.09;34905.64±12361.87 vs 26684.56±12662.24）,差异均有统计学意义（P〈0.05）。2.各基因蛋白表达在临床分期,分化程度和病理类型中均无显著性差异。3.JAK2、HSP基因蛋白表达两者间呈正相关关系（r=0.330,P=0.011）。结论 JAK2、HSP基因蛋白表达上调可能与卵巢癌紫杉醇化疗耐药有一定相关性。     

高表达IL-12卵巢癌细胞的建立

目的 建立高表达IL-12的卵巢癌细胞,为后续IL-12治疗卵巢癌奠定基础。方法 将人卵巢癌细胞株SKOV3分为SKOV3组、SKOV3/GFP组和SKOV3/IL-12组三个实验组,SKOV3组不做任何处理,SKOV3/GFP组给予空载病毒感染SKOV3细胞,SKOV3/IL-12组给予IL-12基因腺病毒感染SKOV3细胞。腺病毒感染SKOV3细胞48 h后,使用荧光显微镜检测三个实验组的感染效率,RT-PCR检测各组SKOV3细胞IL-12 p35、p40 mRNA水平的表达量,ELISA方法检测感染72 h后各组细胞培养液中IL-12的含量。结果 SKOV3/GFP和SKOV3/IL-12组中的SKOV3细胞均可以在荧光显微镜下观察到绿色荧光,而SKOV3组没有观察到绿色荧光,SKOV3/GFP和SKOV3/IL-12组的感染效率分别是（97±1）%和（95±1）%,差异具有统计学意义（P＜0.05）;RT-PCR结果表明,与SKOV3和SKOV3/GFP组相比较,SKOV3/IL-12组可以成功扩增出IL-12 p35、p40亚基,差异具有统计学意义（P＜0.05）;ELISA结果表明,与SKOV3和SKOV3/GFP组比较,SKOV3/IL-12组能够高表达IL-12P70蛋白,差异具有统计学意义（P＜0.05）。结论 成功建立了高表达IL-12的卵巢癌SKOV3细胞,为进一步采用IL-12进行卵巢癌的免疫治疗打下了基础。     

Establishment and characterization of an adriamycin-resistant subline of human small cell lung cancer cells

An adriamycin (ADM)-resistant subline was established by continuous exposure of the SBC-3 cells, a cell line of human small cell lung cancer, to increasing concentrations of ADM, followed by the cloning procedure. The resistant sublines (SBC-3/ADM) thus established were 30-fold more resistant to ADM than the parent SBC-3 cells, in terms of the 70% lethal dose determined by soft agar clonogenic assay. The doubling times of the SBC-3 and SBC-3/ADM cells were 36 h and 22 h, respectively. When transplanted into athymic nude mice, the parent as well as resistant cells formed tumors, and serial passage was successful. Although the transplanted tumors from the two cell lines were very similar in histology, the resistance of the SBC-3/ADM cells to ADM developed in vitro was maintained in serially transplanted tumors. The uptake studies with [3H]daunomycin revealed decreased influx and enhanced active efflux of the drug in the resistant cells, whereas cytogenetic analysis showed that the cell lines had an identical karyotype. These results indicate that ADM resistance may be attributed to alternations in membrane transport, resulting in reduced intracellular accumulation of the drug.     

不良心理应激对人卵巢癌荷瘤裸鼠皮下移植瘤生长及表皮生长因子受体、磷酸化蛋白激酶B、血管内皮生长因子蛋白表达的影响

目的 通过观察不良心理应激人卵巢癌荷瘤裸鼠皮下移植瘤的体积、重量和瘤体组织中表皮生长因子受体（EGFR）、磷酸化蛋白激酶B（p-Akt）、血管内皮生长因子（VEGF）蛋白表达情况的差异,探讨其对卵巢癌生长的影响及可能的分子机制。 方法 购置4～6周龄的雌性BALB/c裸鼠,称重,随机分两组,每组12只。A组：荷瘤组皮下移植人卵巢癌组织瘤块,不给予应激;B组：荷瘤+应激组皮下移植人卵巢癌组织瘤块,给予应激。定期测量皮下移植瘤的体积,结束应激实验后的第2天,处死全部组别（A组、B组）裸鼠,剥离肿瘤予以称重,利用免疫组织化学及Western blotting方法对A、B两组皮下移植瘤组织中的EGFR、p-Akt、VEGF蛋白表达情况进行检测。 结果 荷瘤+应激组皮下移植瘤体积及其重量显著高于荷瘤组（P＜0.01）;免疫组织化学实验提示,荷瘤+应激组中皮下移植瘤组织中的EGFR、p-Akt、VEGF蛋白表达水平高于荷瘤组（P<0.05）;Wester blotting提示,荷瘤+应激组皮下移植瘤组织中EGFR、p-Akt、VEGF蛋白表达水平显著高于荷瘤组（P<0.01）。 结论 不良心理应激可能通过EGFR及其介导的下游PI3K/Akt信号通路来促进卵巢癌的发生、发展。     

紫草素对卵巢癌细胞SKOV3/DDP顺铂耐药的逆转作用

目的:探讨紫草素是否逆转卵巢癌细胞SKOV3/DDP的顺铂耐药效应及其作用机制。方法:采用CCK-8法确定紫草素和顺铂的最佳作用条件,流式细胞术检测细胞的周期分布及凋亡率;Western blot检测周期及凋亡相关调控因子细胞周期蛋白D1(cyclin D1)、周期蛋白依赖性激酶2(CDK2)、P18、p-Rb、Bcl-2、Bax和cleaved caspase-3的蛋白水平。结果:CCK-8实验结果显示,相较于单用顺铂,联合使用紫草素对顺铂耐药卵巢癌细胞SKOV3/DDP的生长抑制作用较为显著。此外,联用紫草素和顺铂可显著抑制细胞周期G_1/S转化,并增加细胞早期凋亡率。Western blot结果显示,相较于顺铂处理组,紫草素和顺铂联用组的cyclin D1、CDK2、p-Rb及Bcl-2的蛋白水平显著降低,而P18、Bax及cleaved caspase-3的蛋白表达显著增加。结论:紫草素可逆转卵巢癌SKOV3/DDP细胞的顺铂耐药效应,其作用机制可能与影响细胞周期及凋亡相关因子的表达,进而抑制细胞活力促进细胞凋亡相关。     

Effects of mesenchymal stem cells harboring the Interferon-β gene on A549 lung cancer in nude mice

Interferon-β (IFN-β) exhibits a tumor-killing effect; however, injection of IFN-β alone for lung cancer is often accompanied by side effects. This study investigated the possibility of using umbilical cord mesenchymal stem cells (MSCs) as cellular carriers of IFN-β.Isolated umbilical cord MSCs were transfected with a lentivirus packaging IFN-β-overexpression plasmid. A549 cells were subcutaneously injected into nude mice to establish a non-small cell lung cancer (NSCLC) mouse model. A total of 50 mice were randomly assigned to 5 different groups: a control group, IFN-β group, IFN-β-MSCs group, MSCs-lentivirus group, and MSCs group. Next, the IFN-β-MSCs, MSCs-lentivirus, and MSCs were injected into the A549 lung cancer-bearing mice in the IFN-β-MSCs, MSCs-lentivirus and MSCs groups, respectively. Mice in the control and IFN-β groups were injected with solvent or IFN-β solution. The tumors in nude mice in the IFN-β and IFN-β-MSCs groups grew at significantly slower rates than tumors in the control group, and tumors in the MSCs-lentivirus and MSC groups also grew slowly. The rates of tumor cell apoptosis in the IFN-β and IFN-β-MSCs groups were significantly higher than those in the MSCs-lentivirus and MSCs groups. The livers, lungs, and kidneys of nude mice in the IFN-β group displayed hyperemia, exudation, and pathological lesions, while those of nude mice in the IFN-β-MSCs group showed no abnormal changes. Both INF-β-MSCs and INF-β inhibited the growth of subcutaneously implanted lung tumors; however, INF-β-MSCs specifically targeted the tumor cells, and did not produce the damage to internal organs caused by the use of INF-β alone.     

Pitfall in chemotherapy for ovarian cancer

Concerning the biological properties of recurrent ovarian cancer, other than drug resistance, we revealed that the expressions of mutant p53 and CD44v6 genes were significantly greater in recurrent ovarian cancer than in those of its primary counterpart. These findings suggest that chemotherapeutic agents may modify some biological characteristics of cancer by altering gene expressions. The biological behavior concerning the metastatic potential of a recurrent disease must be elucidated in order to develop an optional treatment regimen against recurrent tumors. Therefore, we established in-vivo cisplatin-resistant cell lines by repeated administration, in order to find a more suitable model for reflecting the biological aggressiveness of clinically recurrent ovarian cancer following chemotherapy. Chemotherapeutic agents have given a substantial advantage to cancer patients. It must be borne in mind that the cancer cells surviving following chemotherapy possibly present different biological properties from primary cancer cells, and that these properties might be developed by the chemotherapeutic agents.     

miR-502-3p 通过靶向结合 CBL 抑制卵巢癌增殖并诱导凋亡

目的 探究微小 RNA 502-3p (micro RNA 502-3p, miR-502-3p) 通过靶向结合 Casitas B 细胞淋巴 瘤 (Casitas B-cell lymphoma, CBL) 参与卵巢癌增殖和凋亡的机制。 方法 下载 GSE66957、 GSE119056、 TCGA_ OV 卵巢癌相关数据矩阵, 分析 miR-502-3p、 CBL 与卵巢癌的关系; 构建过表达 miR-502-3p、 CBL 的 SKOV3 和 HO8910 细胞系, 分别采用细胞计数试剂盒 ( cell counting kit 8, CCK-8)、 克隆形成实验、 流 式细胞术检测细胞增殖和凋亡情况; 通过荷瘤裸鼠实验, 观察过表达 CBL 对肿瘤生长的影响; 验证 miR502-3p 与 CBL 的靶向关系。 结果 生物信息学分析显示, 卵巢癌组织中 CBL 水平高于癌旁组织, miR-502- 3p 水平低于癌旁组织, CBL 水平与患者预后、 细胞增殖基因表达有关 (P< 0. 05)。 miR-502-3p 与 CBL 存在 靶向关系, 与 Vector 组比较, CBL 组肿瘤的体积及重量增加 (P< 0. 05); 与 miR-NC 组比较, miR-502-3p 组 SKOV3、 HO8910 细胞中 CBL 蛋白表达、 细胞活力、 克隆数降低, 细胞凋亡率升高 (P< 0. 05), 但 CBL 可逆转上述细胞变化。 结论 miR-502-3p 可通过靶向下调 CBL 抑制卵巢癌细胞的增殖, 并诱导其凋亡。     

高转移人卵巢癌裸鼠皮下移植瘤模型的建立及其生物学特性

用人卵巢癌细胞系HO－8910移植探鼠，建立高转移人卵巢癌探鼠皮下移植瘤模型命名为（NSMO），已传代23次，仍保持高转移的特性。共接种BALB/c棵小鼠57只，皮下成瘤率为100％，平均带瘤存活时间为159．9天。在解剖47只裸鼠中有转移瘤鼠42只（89．4％）。最早出现转移的时间为56天。移植瘤组织学和超微结构保持原来人卵巢分化差的浆液性乳头状囊腺癌的形态特征和分泌功能。流式细胞术分析显示DNA指数为1．4，染色体分析显示众数为54（属于超二倍体），显示人类癌症的特征。移植瘤相关标记物检测显示大多数癌细胞雌激素受体和孕激素受体阳性。该模型为转移机制的研究和寻找抗转移药物提供了理想的工具。     

miR-141-3p对卵巢癌的作用及其机制

目的:探究miR-141-3p在卵巢癌中的作用及其相关的分子机制.方法:实时荧光定量PCR检测30例卵巢囊肿和30例卵巢癌组织中miR-141-3p和表皮生长因子受体(EGFR)的表达水平.将SKOV3细胞分为NC组(无转染的SKOV3细胞),miR-141-3p组(SKOV3细胞转染miR-141-3p),LV-EG...