微小RNA与卵巢癌铂类耐药的研究进展

微小RNA(micmRNA,miBNA)是广泛存在于生物体内的一类非编码的小RNA,miRNA是细胞增殖、死亡、应激抗性和脂肪代谢的关键调节因素,体外实验已经证实miRNA在卵巢癌耐药中起重要作用.卵巢癌铂类耐药的产生与发展是十分复杂的过程,研究结果显示,miRNA的表达对卵巢癌细胞株的铂类药物敏感性有着重要作用,能够...     

卵巢癌耐药相关微小RNA的研究进展

越来越多的证据表明,微小RNA(miRNA)的异常表达与肿瘤发生发展、转移及预后等密切相关.最近研究发现,异常表达的miRNA与卵巢癌化疗抵抗相关,提示miRNA将可能成为卵巢癌治疗的新靶点.进一步阐明miRNA与卵巢癌耐药的相关机制将有利于miRNA靶向治疗的研究.     

上皮性卵巢癌中microRNA的研究进展

非编码短序列RNA(microRNA,miRNA)是一类长度约为21～22个核苷酸的短序列、非编码、具有调控作用的单链RNA分子,可以在转录水平后调控mRNA的表达.作为一个重要的基因调节因子,miRNA在肿瘤中发挥癌基因或抑癌基因样作用,与肿瘤癌细胞的增殖、凋亡、转移、耐药等机制密切相关.卵巢癌是严重威胁女性健康的常见恶性肿瘤之一,在女性肿瘤中病死率居第5位,因病灶隐匿,不易早期发现,故发现时多为晚期,5年生存率低.随着miRNA在肿瘤中的深入研究,miRNA在卵巢癌中存在差异表达,其与卵巢癌的作用日渐明朗,有望成为新一代敏感的肿瘤标志物,并通过对其靶基因的研究,最终达到早期诊断及提高卵巢癌治疗效果的目的.     

微小RNA与卵巢癌

微小RNA (miRNA)的异常表达与卵巢癌的发生发展密切相关,其参与调控卵巢癌的发生、侵袭和转移以及抗癌药物耐药性形成等过程.作为一种重要的生物学标志物,miRNA有望成为卵巢癌早期诊断与预后判断的新靶点,为卵巢癌的治疗提供新的途径.     

微小RNA在卵巢癌中的作用

微小RNA( miRNA)在卵巢癌中表达明显改变.基于微阵列芯片检测的卵巢癌相关miRNA表达谱和后续的对个别miRNA的深入研究,发现其与卵巢癌的发生、发展、复发、耐药等密切相关,有望用于卵巢癌早期诊断、复发检测、预后判定及治疗.     

微小RNA与肿瘤诊断

微小RNA (miRNA)能在转录后水平调节mRNA表达。miRNA与胃肠癌、肺癌、乳腺癌、卵巢癌、前列腺癌、胰腺癌和肝癌等多种肿瘤的发生、发展密切相关,而且很多miRNA在肿瘤中表达水平明显异常。miRNA可作为一种标志物用于多种肿瘤的诊断。     

微小RNA与肿瘤诊断

微小RNA（miRNA）能在转录后水平调节mRNA表达。miRNA与胃肠癌、肺癌、乳腺癌、卵巢癌、前列腺癌、胰腺癌和肝癌等多种肿瘤的发生、发展密切相关,而且很多miRNA在肿瘤中表达水平明显异常。miRNA可作为一种标志物用于多种肿瘤的诊断。     

循环血液外泌体miRNA在卵巢癌发生发展中作用及其诊断价值的研究进展

卵巢癌（ovarian cancer,OC）是女性恶性肿瘤死亡的主要原因。由于卵巢癌无症状发展,缺乏早期诊断标志物,大多数患者在晚期才被诊断出来。早期检测卵巢癌可显著提高总生存率,在过去的几十年里,微小RNA（miRNA）在癌症的发展中起着重要的作用,因此引起了极大的关注。miRNA可以在循环血液中稳定存在(如包裹在外泌体中),并可通过外泌体的分泌和转移在肿瘤细胞之间和肿瘤细胞微环境的沟通中发挥重要的作用。此外,外泌体miRNA在卵巢癌中的表达是失调的,可能反映肿瘤的恶性特征。因此评估外泌体来源的循环miRNA可能会为卵巢癌提供一类新的非侵袭性生物标志物。本综述概述了有关外泌体miRNA在卵巢癌发生发展过程中的作用以及循环血液外泌体miRNA作为卵巢癌早期诊断潜在生物标志物的现状。     

微RNA与肿瘤

微RNA(miRNA)是一类非编码的小RNA分子,通过直接抑制基因转录或蛋白质的表达而在器官发育,细胞增殖、分化和凋亡等多种生理过程中发挥关键作用.miRNA异常表达往往导致包括肿瘤在内的多种疾病.研究发现,miRNA在肿瘤发生发展、侵袭转移及肿瘤的诊治中起着重要作用.     

微RNA与肿瘤

微RNA（miRNA）是一类非编码的小RNA分子,通过直接抑制基因转录或蛋白质的表达而在器官发育,细胞增殖、分化和凋亡等多种生理过程中发挥关键作用.miRNA异常表达往往导致包括肿瘤在内的多种疾病.研究发现,miRNA在肿瘤发生发展、侵袭转移及肿瘤的诊治中起着重要作用.     

MicroRNA signatures in human ovarian cancer

Epithelial ovarian cancer (EOC) is the sixth most common cancer in women worldwide and, despite advances in detection and therapies, it still represents the most lethal gynecologic malignancy in the industrialized countries. Unfortunately, still relatively little is known about the molecular events that lead to the development of this highly aggressive disease. The relatively recent discovery of microRNAs (miRNA), a class of small noncoding RNAs targeting multiple mRNAs and triggering translation repression and/or RNA degradation, has revealed the existence of a new level of gene expression regulation. Multiple studies involving various types of human cancers proved that miRNAs have a causal role in tumorigenesis. Here we show that, in comparison to normal ovary, miRNAs are aberrantly expressed in human ovarian cancer. The overall miRNA expression could clearly separate normal versus cancer tissues. The most significantly overexpressed miRNAs were miR-200a, miR-141, miR-200c, and miR-200b, whereas miR-199a, miR-140, miR-145, and miR-125b1 were among the most down-modulated miRNAs. We could also identify miRNAs whose expression was correlated with specific ovarian cancer biopathologic features, such as histotype, lymphovascular and organ invasion, and involvement of ovarian surface. Moreover, the levels of miR-21, miR-203, and miR-205, up-modulated in ovarian carcinomas compared with normal tissues, were significantly increased after 5-aza-2'-deoxycytidine demethylating treatment of OVCAR3 cells, suggesting that the DNA hypomethylation could be the mechanism responsible for their overexpression. Our results indicate that miRNAs might play a role in the pathogenesis of human EOC and identify altered miRNA gene methylation as a possible epigenetic mechanism involved in their aberrant expression.     

Differential microRNA Expression by Solexa Sequencing in the Sera of Ovarian Cancer Patients

MicroRNAs are a class of small noncoding RNA which play important regulatory roles in a variety of cancers.MiRNA-specific expression profiles have been reported for several pathological conditions. In this study, wecombined large scale parallel Solexa sequencing to identify 11 up-regulated miRNAs and 19 down-regulatedmiRNAs with computational techniques in the sera of ovarian cancer patients while using healthy serum as thecontrol. Among the above, four miRNAs (miR-22, miR-93, miR-106b, miR-451) were validated by quantitativeRT-PCR and found to be significantly aberrantly expressed in the serum of ovarian cancer patients (P<0.05).There were no significant differences between samples from cancer stage Ⅰ/Ⅱ and Ⅲ/Ⅳ. However, the levelsof miR-106b (p=0.003) and miR-451 (p=0.007) were significantly different in those patients under and over 51yearsof age. MiR-451 and miR-93 were also specific when analyzed with reference to different levels of CA125.This study shows that Solexa sequencing provides a promising method for cancer-related miRNA profiling, andselectively expressed miRNAs could be used as potential serum-based biomarkers for ovarian cancer diagnosis.     

Altered microRNA expression in cisplatin-resistant ovarian cancer cells and upregulation of miR-130a associated with MDR1/P-glycoprotein-mediated drug resistance

microRNAs (miRNAs) are short non-coding RNA molecules which are involved in the regulation of various biological processes. Drug resistance has become a major obstacle to successful chemotherapy of ovarian cancer. The aim of this study was to investigate microRNA expression profiles in cisplatin-resistant ovarian cancer cells and the role of miR-130a in regulating drug resistance. Analysis of differentially expressed miRNAs between SKOV3 and SKOV3/CIS cells was assessed by miRNA microarrays. Target prediction of miRNAs was determined with the help of PicTar or TargetScan. Among these miRNAs, the expression of miR?130a was verified using qRT-PCR. The expression of MDR1 mRNA and P-glycoprotein (P-gp) after cellular transfection was examined using qRT-PCR and western blotting, respectively. Cisplatin sensitivity was detected by the MTT assay. We indentified 35 downregulated and 54 upregulated miRNAs in SKOV3/CIS compared to those in SKOV3. We found that miR-130a was upregulated in SKOV3/CIS compared to the parental SKOV3 cells, and PTEN was predicted to be the potential target of miR-130a. Moreover, downregulation of miR-130a could inhibit MDR1 mRNA and P-gp expression and overcome the cisplatin resistance in SKOV3/CIS cells, which indicated that miR-130a may be associated with MDR1/P-gp-mediated drug resistance and plays the role of an intermediate in drug-resistance pathways of PI3K/Akt/PTEN/mTOR and ABC superfamily drug transporters in SKOV3/CIS cells. This study provides important information for the development of targeted gene therapy for reversing cisplatin resistance in ovarian cancer.