H3K9Ac在卵巢上皮性肿瘤中的表达及其临床意义

目的 研究组蛋白H3赖氨酸残基9位乙酰化（H3KgAc）在卵巢上皮性肿瘤中的表达及其与卵巢癌组织学分级、临床分期之间的关系。方法 采用免疫组织化学ABC法检测20例良性、16例交界性、40例恶性卵巢上皮性肿瘤中H3K9Ac的表达情况，并分析其与临床病理指标间的关系。结果 ①H3K9Ac在良性、交界性、恶性卵巢上皮性肿瘤中的表达逐渐降低，差异有显著统计学意义（P〈0．01）；②与粘液性囊腺癌相比，H3KgAc在浆液性囊腺癌中表达较低，差异有统计学意义（P〈0．05）；③H3KgAc的表达与卵巢上皮性癌的组织分化程度及临床分期有关，在Ⅲ、Ⅳ期卵巢癌中H3KgAc的表达明显低于Ⅰ、Ⅱ期卵巢癌（P〈0．01）；随着组织分化程度降低，H3KgAc表达也逐渐降低，两两比较差异有统计学意义（P〈0．05）。结论 H3KgAc在良性、交界性、恶性卵巢上皮性肿瘤中的表达差异显著，且随着卵巢上皮性癌恶性程度的增高，表达逐渐降低，H3K9Ac可能为卵巢上皮性肿瘤的良恶性及其预后判断提供一个新的生物学指标。     

Wnt2B及PAI-1在上皮性卵巢癌中的表达及临床意义

目的 通过检测Wnt2B与PAI-1在上皮性卵巢癌中的表达,分析两者与上皮性卵巢癌侵袭转移及临床病理之间的关系,以探讨两种基因在上皮性卵巢癌的表达及临床意义.方法 应用免疫组化(SP法)检测2008年1月到2013年6月在本院行手术切除的上皮性卵巢癌82例和良性卵巢上皮瘤10例患者组织中Wnt2B和PAI-1蛋白的表达情况,分析上皮性卵巢癌的年龄、组织学类型、细胞学分级、手术病理分期、肿瘤病灶大小、盆腔转移灶大小、大网膜转移、淋巴结转移、远处转移、残留病灶大小等临床病理因素与两个基因的表达关系;分析上皮性卵巢癌患者癌组织中Wnt2B与PAI-1的表达关系.结果 上皮性卵巢癌患者癌组织中Wnt2B的阳性表达率为12.2％(10/82),低于良性卵巢上皮瘤患者瘤组织的70％ (7/10)(P＜0.05);上皮性卵巢癌患者癌组织中PAI-1的阳性表达率为76.8％(63/82),高于良性卵巢上皮瘤患者瘤组织的20％ (2/10) (P＜0.05).PAI-1的表达与手术病理分期、细胞学分级、大网膜转移、盆腔转移灶大小有关(均P＜0.05),而与患者年龄、组织学类型、肿瘤病灶大小、淋巴结转移、远处转移、残留病灶大小无关(均P＞0.05);Wnt2B表达与手术病理分期、大网膜转移有关(均P＜0.05),与患者年龄、组织学类型、细胞学分级、肿瘤病灶大小、盆腔转移灶大小、淋巴结转移、远处转移、残留病灶大小无关(均P＞0.05).上皮性卵巢癌患者癌组织中Wnt2B与PAI-1的表达呈负相关(r=-0.847,P＜0.05).结论 Wnt2B在上皮性卵巢癌的发病机制中可能发挥一定的作用.PAI-1的表达与上皮性卵巢癌的发生、发展、浸润、转移有关.     

卵巢上皮性肿瘤中Skp2、p27kipl、E-cad的表达

目的检测Skp2、p27kipl和E-cad在卵巢上皮性肿瘤中的表达情况及其相互关系。方法采用免疫组化SP法，检测99例卵巢上皮性肿瘤组织中Skp2、p27kipl及E-cad的表达。结果p27kipl在卵巢良性肿瘤、交界性肿瘤的表达率分别为76．5％、70．6％高于卵巢癌29．2％（P〈0．05），在早期癌中的表达高于晚期癌（P〈0．05）。Skp2在卵巢良性肿瘤、交界性肿瘤的表达率分别为0、23．5％，均低于卵巢癌50．8％（P〈0．05），在早期癌的表达低于晚期癌（P〈0．05）。卵巢癌中skp2表达与组织分化有关，在低分化癌的阳性表达率高于高分化癌（P〈0．05），在组织学类型方面，浆液性癌中skp2的阳性表达率高于非浆液性癌（P〈0．05）。E—cad在良性肿瘤、交界性肿瘤和卵巢癌表达率分别为88．2％、82．4％、55．4％，恶性组低于良性组（P〈0．05）。E—cad在早期癌的表达率高于晚期癌（P〈0．05）。Skp2表达与p27kipl表达呈负相关（P〈0．05），E-cad表达与p27kipl表达呈正相关（P〈0．05），而E-cad表达与Skp2表达则呈负相关（P〈0．05）。结论skp2过度表达与p27kipl表达减少可能与卵巢上皮性肿瘤的发生发展密切相关，而E-cad在晚期卵巢癌中表达降低可能反映了卵巢癌分化程度的降低。     

TopoⅡα和抑癌基因PTEN在卵巢上皮性癌中的表达及其意义

目的探讨拓扑异构酶Ⅱα（TopoⅡα）和PTEN蛋白在卵巢上皮性癌组织中的表达及与临床病理特征的关系。方法应用免疫组化法检测56例卵巢上皮性癌组织,30例良性卵巢肿瘤及15例正常卵巢组织中TopoⅡα和PTEN蛋白的表达。结果 （1）TopoⅡα在良性卵巢肿瘤组织及正常卵巢组织中的阳性表达率为16.7%、13.3%,显著低卵巢癌组织的53.6%,差异有显著性（P〈0.05）;TopoⅡα表达与卵巢癌临床分期、淋巴结转移有关,而与年龄、病理类型、组织学分级无关。（2）PTEN蛋白在卵巢癌组织中的阳性表达率为33.9%,低于正常卵巢和良性上皮肿瘤组织的93.3%,100%（P〈0.05）;PTEN蛋白表达与卵巢癌临床分期、组织学分级、淋巴结转移有关,而与年龄、病理类型无关。（3）卵巢癌组织中TopoⅡα和PTEN蛋白间的表达呈负相关（r=-0.507,P〈0.05）。结论 TopoⅡα和PTEN蛋白的异常表达可能与上皮性卵巢癌的发生、发展、侵袭性和预后相关,通过对它们的检测可以对卵巢癌的预后及化疗提供理论依据。     

Ki-67和CD44v5在卵巢癌中的表达和临床意义

目的 研究ki-67和CD44v5在卵巢癌中的表达及临床意义。方法 用免疫组化sp法研究ki-67和CD44v5在40例卵巢癌手术切除标本及10例卵巢上皮良性肿瘤中的表达。结果 40例卵巢癌中，ki-67和CD44v5的阳性表达率分别为77．5％和47．5％，远高于在卵巢上皮良性肿瘤中的表达30．0％和20．0％。且随着肿瘤病理分化程度的降低，ki-67、CD44v5阳性表达率均呈增高趋势；ki-67在卵巢腺癌中的阳性表达率明显高于透明细胞癌、内膜样癌（P〈0．05）；CD44v5的阳性表达率与表达强度伴淋巴转移者显著高于无淋巴转移者（P〈0．01）；两者呈正相关。结论 ki-67和CD44v5在卵巢癌中的表达对卵巢癌的诊断、治疗方式的选择、手术范围的确定、及术后防治复发、化疗药物的应用，具有重要的指导意义。     

血清中人附睾上皮分泌蛋白4的测定与卵巢上皮性肿瘤患者临床病理特征的关系

为探讨卵巢上皮性肿瘤患者血清人附睾上皮分泌蛋白4（HE4）水平的变化,以及与临床病理特征的关系,采用酶联免疫吸附试验（ELISA）检测21例良性卵巢上皮肿瘤患者、12例交界性卵巢上皮肿瘤患者和49例卵巢癌患者血清HE4水平,并分析其水平与临床病理特征的关系。卵巢癌组血清HE4水平（中位数123.00pmol/L）明显高于交界性卵巢上皮肿瘤组（中位数41.20pmol/L）和良性卵巢上皮肿瘤组（中位数32.80pmol/L）;血清HE4水平与卵巢上皮性癌患者是否绝经、年龄及有无淋巴结转移无关（P〉0.05）,而与患者的临床FIGO分期（Ⅰ＋Ⅱ、Ⅲ＋Ⅳ）、病理组织学类型及有无腹水有关（P〈0.05）,浆液性癌（中位数198.50pmol/L）和子宫内膜样癌患者的血清HE4水平（中位数139.25pmol/L）明显高于黏液性癌患者（中位数30.95pmol/L）（U值分别为17.00和2.00,P〈0.01）。血清HE4水平与卵巢上皮性癌临床病理特征密切相关,并有望成为卵巢上皮性肿瘤恶变的标志物。     

PTEN蛋白和FHIT蛋白在上皮性卵巢癌中的表达及临床病理意义

目的检测抑癌基因蛋白PTEN、FHIT表达在卵巢癌发展中的作用及相关病理机制。方法采用免疫组化法检测45例卵巢癌组织、10例卵巢交界性肿瘤、10例卵巢良性肿瘤、5例正常卵巢组织中PTEN和FHIT蛋白表达，并比较这两种蛋白表达与临床病理特征的关系。结果卵巢癌和交界性卵巢肿瘤组织中PTEN蛋白和FHIT蛋白表达显著低于卵巢囊肿和正常卵巢（P〈0．05），在上皮性卵巢癌中这两种蛋白表达与组织分化程度正相关（P〈0．05），它们表达降低或失活与卵巢癌淋巴结转移相关（P〈0．005），但与组织学类型无显著相关性。PTEN蛋白表达与恶性肿瘤临床分期负相关．FHIT蛋白表达与临床分期无显著相关性。这两种蛋白在上皮性卵巢癌中表达的相关性有统计学意义（P=0．0343）。结论在卵巢癌发生过程中PTEN蛋白表达降低起到重要作用，预示着卵巢癌的不良预后；FHIT蛋白缺失是恶性上皮性卵巢肿瘤的特征，其表达缺失在卵巢肿瘤的发生发展中起一定作用，可能与上皮性卵巢癌的恶性进展及转移有关．这两种蛋白可能协同促进卵巢癌的发生、发展、浸润及转移。     

肿瘤坏死因子-α在卵巢肿瘤患者腹水中的表达及意义

目的 探讨卵巢肿瘤患者腹水中肿瘤坏死因子-α(TNF-α)与卵巢癌之间的关系,探讨其对腹水性质鉴别的价值.方法 采用酶联免疫吸附法(ELISA)检测59例卵巢上皮性肿瘤、9例原发性腹膜癌、6例卵巢子宫内膜异位囊肿患者腹水TNF-α水平.结果 腹水TNF-α水平在卵巢恶性上皮性肿瘤、卵巢交界性肿瘤、原发性腹膜癌中的水平明显高于卵巢良性上皮性肿瘤、卵巢子宫内膜异位囊肿,且与肿瘤的恶性行为包括临床分期、组织分化程度、淋巴转移及腹水量等有关.结论 腹水TNF-α对诊断卵巢癌有较高的敏感性和特异性,可能成为卵巢恶性肿瘤的标志物.     

P16、P53和CyclinD1蛋白在卵巢浆液性肿瘤中的表达及意义

目的 探讨浆液性卵巢上皮性肿瘤中P16、P53和CyclinD1蛋白的表达情况及意义.方法 应用免疫组化法对2010-2011年本院45例浆液性卵巢癌(低级别19例,高级别26例)、25例卵巢交界性浆液性囊腺瘤及21例卵巢浆液性囊腺瘤组织进行P16、P53、CyclinDl蛋白检测,并分析其临床病理意义.结果 P16在良性、交界性与癌组的阳性表达率分别为24％、72％及89％,良性肿瘤组与交界性和癌组之间差异有统计学意义(P＜0.05).P53在良性、交界性与恶癌组的阳性表达率分别为5％、4％及42％,良性和交界性肿瘤组与癌组之间差异有统计学意义(P＜0.05).CyclinD1在良性、交界性与癌组的阳性表达率分别为10％、64％及47％.良性肿瘤组、交界性肿瘤组与癌组之间差异均有统计学意义,P＜0.05.P53、CyclinD1在卵巢浆液性癌高低级间别比较差异均有统计学意义,两者表现为负相关,r=0.211.结论 P16的阳性表达常见于卵巢交界性浆液性囊腺瘤和卵巢浆液性癌中,P53的阳性表达更多见于高级别卵巢浆液性癌中,CyclinD1的阳性表达更多见于卵巢交界性浆液性肿瘤与低级别浆液性癌组织中.卵巢高级别癌与低级别癌的发病机制不同.     

卵巢上皮性肿瘤神经内分泌细胞增殖与凋亡研究

目的： 观察卵巢上皮性肿瘤组织中神经内分泌细胞（NECs）的形态特点及增殖与凋亡状况，以探讨其生物学及临床意义。 方法： 手术切除的卵巢上皮性肿瘤标本79例，其中良性20例，交界性18例，恶性41例，正常卵巢组织22例作对照，采用嗜铬素A（CgA）免疫组化染色显示NECs，并进行CgA/Ki67及TUNEL/CgA双重染色，观察NECs的增殖与凋亡状况。 结果： 卵巢上皮性肿瘤组织NECs的阳性率、分布范围及染色强度均高于正常卵巢组织。卵巢上皮性肿瘤中NECs形态多样，具有神经元样突起，延伸到毗邻细胞或基底膜，NECs之间亦有突起相互接触。双重免疫组化染色显示NECs均呈TUNEL染色阴性，部分细胞Ki67染色阳性。 结论： 卵巢上皮性肿瘤组织中NECs与肿瘤细胞一样可增殖，但不发生凋亡，其分泌产物可促进周围非NECs的增殖，抑制其凋亡。     

过氧化物酶体增殖物激活受体β与上皮性卵巢癌的关系

目的:探讨过氧化物酶体增殖激活物受体β(PPARβ)的表达及其与上皮性卵巢癌临床病理特征间的关系。方法:用免疫组织化学染色和半定量RT-PCR法检测PPARβ在正常卵巢组织和卵巢癌组织的表达。结果:PPARβ在上皮性卵巢癌和非癌组织均有表达,PPARβ的表达定位于细胞质中,在正常卵巢、卵巢交界性肿瘤、浆液性囊腺癌中PPARβ表达阳性率分别为20%、50%及89·1%。在浆液性囊腺癌中表达明显高于交界性肿瘤和正常卵巢组织(P<0·05),且与临床分期、组织学分级和淋巴结转移有关(P<0·05)。结论:PPARβ表达水平增高可能与卵巢上皮癌的分化转移有关。     

卵巢上皮癌中细胞外信号调节激酶的表达及其与预后的关系

目的: 探讨磷酸化细胞外调节激酶(p-ERK)在卵巢上皮癌组织中的表达及其与肿瘤患者预后之间的关系。方法: 应用Western印迹方法分别测定正常卵巢组织、良性卵巢组织和卵巢上皮癌组织中p-ERK的含量;收集卵巢上皮癌患者的临床资料;应用Kaplan-Meier法和Cox回归对卵巢上皮癌患者进行生存分析。结果: (1)卵巢上皮癌组织中的p-ERK含量明显高于良性卵巢组织和正常卵巢组织(P<0.01),Ⅲ~Ⅳ期卵巢上皮癌组织中p-ERK含量明显高于I~II期(P<0.01),良性卵巢组织中p-ERK含量与正常卵巢组织相比无显著差异(P>0.05);(2)低分化卵巢上皮癌组织中的p-ERK含量高于中、高分化(P<0.01);(3)在不同病理类型卵巢癌中,与浆液性卵巢上皮癌组织相比,未分化腺癌组织中p-ERK含量与其相仿(P>0.05),而黏液性卵巢上皮癌和卵巢子宫内膜样癌组织中p-ERK含量较低(P<0.05);(4)p-ERK含量与生存时间呈负相关,p-ERK含量高的卵巢上皮癌患者生存时间短;(5)卵巢上皮癌患者的生存时间与p-ERK含量、残余灶、肿瘤分期、肿瘤分级以及化疗的疗程有着密切关系(P<0.05),而与肿瘤的病理类型没有相关性(P>0.05)。结论: p-ERK可能是卵巢上皮癌发病机制一个重要的调节激酶;测定p-ERK水平可能对卵巢上皮癌患者预后有预测价值。     

Differential gene expression in ovarian carcinoma: identification of potential biomarkers

Ovarian cancer remains the fifth leading cause of cancer death for women in the United States. In this study, the gene expression of 20 ovarian carcinomas, 17 ovarian carcinomas metastatic to the omentum, and 50 normal ovaries was determined by Gene Logic Inc. using Affymetrix GeneChip HU_95 arrays containing approximately 12,000 known genes. Differences in gene expression were quantified as fold changes in gene expression in ovarian carcinomas compared to normal ovaries and ovarian carcinoma metastases. Genes up-regulated in ovarian carcinoma tissue samples compared to more than 300 other normal and diseased tissue samples were identified. Seven genes were selected for further screening by immunohistochemistry to determine the presence and localization of the proteins. These seven genes were: the beta8 integrin subunit, bone morphogenetic protein-7, claudin-4, collagen type IX alpha2, cellular retinoic acid binding protein-1, forkhead box J1, and S100 calcium-binding protein A1. Statistical analyses showed that the beta8 integrin subunit, claudin-4, and S100A1 provided the best distinction between ovarian carcinoma and normal ovary tissues, and may serve as the best candidate tumor markers among the seven genes studied. These results suggest that further exploration into other up-regulated genes may identify novel diagnostic, therapeutic, and/or prognostic biomarkers in ovarian carcinoma.     

p53 protein expression in putative precursor lesions of epithelial ovarian cancer

p53 protein expression has been studied in epithelial inclusion cysts adjacent to and contralateral to serous carcinoma of the ovary and compared to epithelial inclusion cysts associated with borderline tumours and in normal ovaries. Atypia was found in epithelial inclusion cysts in eight of the thirteen advanced (stage III) serous ovarian carcinomas. Of these eight with atypical epithelial inclusion cysts, five showed immunoreactivity for p53. In the borderline tumours and normal ovaries no atypia in such cysts was found. p53 expression was also seen more frequently in surface epithelium associated with ovarian serous adenocarcinoma (ten of 13) than in normal ovaries (one of 13). We postulate that focal areas of atypia (ovarian intra-epithelial neoplasia) in epithelial inclusion cysts are the precursors of ovarian malignancy. In some cases, at least, p53 protein expression may precede overt cytological abnormalities.     

Loss of expression of EphB1 protein in serous carcinoma of ovary associated with metastasis and poor survival

Aberrant expression of receptors tyrosine kinase of Eph gene in human cancers is extensively documented. We previously found that EphB1 subtype is down-regulated in gastric cancer and colorectal cancer. Fore the more, decreased expression of EphB1 is related to invasion and metastasis in cancers. There is no published data regarding the role of EphB1 in ovarian cancer, which is the focus of the present study. The expression of EphB1 protein was determined in tissues from 74 patients with serous ovarian carcinoma and 12 normal ovarian epithelial tissues. The expression level of EphB1 protein in serous ovarian carcinoma was analyzed with respect to clinicopathological parameters and survival. EphB1 protein was positively stained in 12 normal ovarian epithelial samples, and negatively stained in 32 out of 74 (43.2%) serous ovarian cancers. Loss of expression of EphB1 protein was associated with higher tumor grade (P = 0.006), metastasis (P = 0.049) and high proliferative index Ki67 expression (P = 0.022), but not with FIGO stage (P = 0.0937), age at diagnosis (P = 0.624), and diameter of carcinoma (P = 0.108). In addition, loss of EphB1 protein in serous ovarian carcinoma was associated with a significantly worse overall survival (P = 0.015). Our data indicate that loss of EphB1 protein is associated with metastasis and poorer survival in patients with serous ovarian cancer. EphB1 may be used as a prognostic marker and a therapeutic target in serous ovarian carcinoma.     

整合素α6β1和CD44V4在卵巢上皮癌中表达及相关性分析

目的 通过检测上皮癌病理组织及正常卵巢组织中整合素α6β1和CD44V4表达情况,探讨其表达特点与临床病理特征的相关性。方法 收集2015年1月~2016年12月手术切除的20例正常卵巢组织、40例卵巢上皮良性肿瘤及65例卵巢上皮癌组织,利用免疫组织化学法检测整合素α6β1和CD44V4的表达水平,结合病理组织特征进行相关性分析。结果 卵巢上皮癌组织中整合素α6β1和CD44V4的表达水平显著高于正常卵巢及上皮良性肿瘤组织,差异有统计学意义（P＜0.05）,且在不同病理分期及分化程度的卵巢上皮癌组织之间的差异有统计学意义（P＜0.05）;但在不同组织学分型病理组织中差异无统计学意义（P＞0.05）;α6β1和与CD44V4在卵巢上皮癌组织中的表达存在明显正相关（r=0.599,P＜0.05）。结论 整合素α6β1和与CD44V4在卵巢上皮癌组织中高表达且有相关性,可作为卵巢上皮癌发展的分子标志物。     

Increased expression of fascin, motility associated protein, in cell cultures derived from ovarian cancer and in borderline and carcinomatous ovarian tumors

Fascin bundles actin microfilaments within dynamic cellular structures such as microspikes, stress fibers and membrane ruffles. Fascin overexpression induces membrane protrusions and increased cell motility, and is highly expressed in various transformed cells, and in specialized normal cells including neuronal, endothelial and dendritic cells. In breast cancer, fascin expression correlates with high-grade tumors. To investigate whether fascin might be a predictor factor for ovarian cancer progression, eighteen cell cultures derived from ovarian cancer, and thirty four archival paraffin-embedded material of normal versus borderline and carcinomatous ovaries were stained by immunocytochemistry and immunohistochemistry with fascin Mab 55K-2. Overall expression of the fascin protein was found in 50% (9/18) of cell cultures derived from original samples of ovarian tumors. Expression of fascin protein was found in 67% (6/9) of cell cultures derived from patients diagnosed with stage IV disease, and 33% (3/9) of cell cultures from patients diagnosed with stage II/III. There was no clear relationship between fascin expression and histologic types, tumor grade, or DNA ploidy. However, 75% of cell cultures, which developed into a xenograft after intraperitoneal inoculation, showed fascin expression, while 86% of non-tumorigenic cell cultures did not show fascin expression. Expression of fascin in these established ovarian tumor cell cultures was significantly associated with the ability for these cells to grow intraperitoneally (P<0.05). Furthermore, fascin was never expressed in normal epithelial ovarian tissues, but was present in all pathologic ovaries. Both diffuse and focal patterns were observed in borderline ovarian tumors (67% and 33%), advanced primary ovarian cancer (67% and 33%) and metastatic ovarian cancer (89% and 11%). Therefore, our data suggest that fascin could serve as a prognostic factor for abnormal ovarian epithelial pathology and could be a novel target for the treatment of ovarian cancer.     

Increased Immunostaining of Fibulin-1, an Estrogen-Regulated Protein in the Stroma of Human Ovarian Epithelial Tumors

Fibulin-1, an extracellular matrix protein, is secreted by human ovarian metastatic cancer cell lines under estrogen stimulation. Fibulin-1 expression was quantified by immunohistochemistry and computer-aided image analysis in 44 human ovarian epithelial tumors and 14 normal ovaries. The fibulin-1 staining intensity in proximal stroma, close to the surface of epithelial cells and tumor cells, progressively increased from normal ovaries to serous carcinomas. In all lesions, excluding cystadenomas, fibulin-1 accumulation was higher in proximal stroma than in distant stroma. In situ hybridization demonstrated strong fibulin-1 gene expression in epithelial cells of serous ovarian carcinomas and some cysts. The weak expression of fibulin-1 RNA in some stromal cells of these tumors could not explain the strong fibulin-1 protein accumulation in tumor stroma, which was therefore mostly produced by tumor epithelial cells. In carcinomas, fibulin-1 staining was not correlated with the percentage of estrogen receptor-α (ERα)-stained nuclei but was inversely correlated with the progesterone receptor. However, in cystadenomas and borderline tumors, both fibulin-1 and ERα protein levels increased, in comparison with normal ovaries, suggesting an effect of estrogens in the early steps of tumorigenesis. This fibulin-1 overexpression, demonstrated in vivo in ovarian carcinomas, might be a useful indicator for predicting cancer risk and/or aggressiveness.     

MiR-191 inhibits TNF-α induced apoptosis of ovarian endometriosis and endometrioid carcinoma cells by targeting DAPK1

Emerging evidence showed that miRNA dysregulation is involved in the development of endometriosis and may contribute to pathological process of endometriosis associated ovarian cancer (EAOC). miR-191 is one of the most differentially expressed miRNAs in pairwise comparisons among healthy controls, endometriosis, and EAOC patients. However, its regulative network in endometriosis and EAOC are still not clear. This study explored the role of miR-191 in TNF-α induced cell death in ovarian endometriosis and endometrioid carcinoma cells. Based on tissues samples collected from healthy controls, endometriosis, and EAOC patients, this study verified significantly higher expression of miR-191 in endometriosis and endometrioid cancer. Interestingly, we also observed inverse expression trend between miR-191 and DAPK1, a positive mediator of programmed cell death. By conducting luciferase assay, we confirmed miR-191 can directly target DAPK1 and regulate its expression. Functionally, we also found DAPK1 can promote TNF-α induced cell death. DAPK1 knockdown in endometriosis CRL-7566 cells can weaken its response to TNF-α induced cell death, while its overexpression in endometrioid cancer cells CRL-11731 enhanced the response. These functions of DAPK1 can be directly modulated by miR-191. Therefore, the miR-191-DAPK1 axis may play an important role modulating the response of ovarian endometriosis and endometrioid carcinoma cells to death-inducers and might contribute malignant transformation of endometriosis.