微核糖核酸在肿瘤血管生成中的调节作用

微核糖核酸(microRNAs,miRNAs)是广泛存在于真核生物中的一类短小的、不编码蛋白质的RNA家族,由18-25个核苷酸组成的单链RNA。研究表明microRNAs对肿瘤的发生发展具有重要的调节作用。肿瘤血管生成是实体瘤侵袭转移的关键步骤,抗肿瘤血管生成的治疗已成为当前研究的焦点,已有研究表明,microRNAs参与肿瘤血管生成的调节作用,通过对肿瘤血管生成相关因子的调控,影响肿瘤生成。     

微核糖核酸对血管生成相关因子的调节作用

微核糖核酸(microRNAs,miRNAs)是广泛存在于真核生物中的一类短小的、非编码的单链RNA,由18～25个核苷酸组成,在调节细胞增殖、分化、凋亡和肿瘤发生等多种生物学过程中起重要作用.血管生成过程中受到多种血管生成因子的调控作用,近期研究表明,microRNAs参与血管生成相关因子的调节,进而影响血管生成,然而具体的功能以及作用机制仍需探讨.进一步研究microRNAs对血管生成相关因子的调控作用,为心血管疾病和肿瘤的治疗提供新的理论基础.     

MicroRNAs与多潜能干细胞的研究进展

microRNAs(miRNAs)是一类内源性非编码小RNA,通过调控基因表达来参与生命过程中的一系列重要进程。越来越多的证据表明,miRNAs参与了几乎所有生物代谢过程,其胚胎干细胞的自我更新与分化和在多能干细胞(iPSCs)中的诱导调节作用也日益受到关注。该文介绍了miRNAs的生成、检测方法以及miRNAs对胚胎干细胞(ESCs)及诱导多能性干细胞的调控作用,并对miRNAs的应用前景进行了展望。     

microRNAs在肌肉中的作用研究进展

microRNAs是一类非蛋白质编码小RNA,通常作用于靶基因mRNA的3′-UTR区引起靶基因的翻译抑制或降解。microRNAs的表达具有组织特异性,骨骼肌和心肌中有特异microRNAs的表达。microRNAs在肌肉的增殖、分化等发育过程中发挥重要的调节作用,并且microRNAs的表达异常与某些肌肉疾病的病理过程有关。现就microRNAs在肌肉中的作用研究进展作一综述。     

微RNA参与调控肿瘤血管生成

肿瘤血管生成是由多种因子参与调控的复杂过程,对肿瘤的生长、侵袭和转移起着关键作用.微 RNA(microRNA, miRNA)是一段长约22 nt的非编码RNA序列,参与调节细胞增殖、分化、凋亡,肿瘤发生、发展等多种生命活动.认识miRNA与肿瘤血管生成的关系不但能加深对血管生成分子机制的理解,同时对阐明 miRNA的功能具有重要意义.     

MicroRNA与肿瘤血管生成

microRNA（miRNA）是近年来发现的一类长度约为22个核苷酸的非编码小分子RNA.它主要通过与靶标基因3′UTR的完全或不完全配对,降解靶标基因mRNA或抑制其翻译,从而参与多种生命活动.血管生成在肿瘤的发生、发展过程中起着重要的作用.实验证据表明,miRNAs可通过调控其靶标基因参与的信号通路,影响肿瘤血管的生成.本文主要介绍近年来miRNAs与血管生成相关性研究的进展.     

microRNAs与血管系统发生及疾病的研究进展

microRNAs(miRNAs)是新近发现的一类长约19-25个核苷酸的内源性微小RNA,通过与靶mRNA的5'或3'的非编码区互补结合而使靶mRNA翻译抑制或降解,在细胞增殖、分化和凋亡,胰岛素分泌,脂肪代谢及肿瘤的发生发展等多种生物学过程中起重要作用.血管是一个复杂的封闭循环性系统,其发育和疾病的发生受到多基因的调控和多因素的影响.近期的研究表明,miRNAs与血管系统的发育及其疾病的发生具有密切的关系.     

微小RNA通过调控肿瘤血管形成影响肿瘤转移

肿瘤转移的过程是一个连续的、相互关联的级联事件,整个过程受多因素、多基因调控。血管形成是肿瘤转移的前提和基础,抑制肿瘤血管生成是控制肿瘤转移的一个可行策略。微小RNA(micro RNAs,mi RNAs)是一类非编码的小分子RNA,可在转录后水平调控肿瘤血管生成,在肿瘤的转移过程中起着至关重要的作用。本文主要就mi RNAs调控肿瘤血管形成参与肿瘤转移过程中的最新研究进展进行了综述。     

microRNA-378 与肿瘤血管生成的研究进展

微小RNA(MicroRNAs,mi RNAs)是真核生物中一类长度约为21到23个核苷酸的非编码小分子单链RNA。mi RNA通过与靶m RNA 3′UTR(3′-untranslated region,3′非编码区)完全或不完全结合,抑制翻译或直接诱导其降解,发挥转录后负调控作用。mi RNA参与机体多种生理和病理过程,且可通过调控其靶标基因参与各种信号通路,影响血管生成。mi R-378属于诸多mi RNAs中的一种。目前已知mi R-378的研究主要集中在肿瘤发生及血管生成、心血管疾病和脑缺血等病理过程,其中与肿瘤发生及血管生成相关研究居多。mi R-378在不同肿瘤中的发挥的作用也不一样,在脑胶质瘤,肺癌,横纹肌肉瘤等肿瘤中发挥促癌基因的作用,在卵巢癌,胃癌,大肠癌等肿瘤中发挥抑癌基因的作用。但是,mi R-378调节肿瘤血管生成的作用机制还有待于深入研究。本文主要对mi R-378在四种肿瘤(脑胶质瘤、肺腺癌、卵巢癌和横纹肌肉瘤)中调控血管生成的相关性研究进展进行综述,以期为这些疾病的治疗和预防提供一种新的思路。     

内皮细胞增殖抑制因子研究进展

内皮细胞过度增殖引起的病理性血管生成是肿瘤、类风湿性关节炎等发病的关键环节。内皮细胞增殖由血管内皮细胞生长因子等促血管生成因子提供促增殖信号,而新近发现的多种内皮增殖抑制因子,如血管内皮抑素、血管抑素、血小板反应蛋白-1、微囊蛋白1、某些microRNAs和某些抑癌基因等,则通过抑制促增殖信号、调节细胞周期、诱导细胞凋亡等途径下调内皮细胞的增殖及血管生成。内皮增殖抑制因子可望成为病理性血管生成防治的新靶点。     

MicroRNA在肿瘤发生发展和诊断中作用的研究进展

microRNA是一类由内源基因编码的长度约为18-25个核苷酸的非编码单链RNA分子,可以与靶基因mRNA的3'非编码区结合,通过降解靶m RNA或(和)抑制靶m RNA转录后翻译调节靶蛋白的生成,从而发挥其生物学作用。目前,在人体基因组内发现的microRNA已经超过2500多个,可能调节着人类1/3的基因,在维持正常干细胞功能、调控细胞增殖分化及恶性肿瘤发生过程中均起重要作用。既往的研究表明microRNA与基因之间相互调控的失衡导致肿瘤的发生。从分子水平上研究microRNA与肿瘤发生的关系,检测microRNA与肿瘤相关基因表达情况的改变,分析肿瘤组织和血清中microRNA表达量与肿瘤分型的关系,将有利于肿瘤的病因学研究,早期发现和肿瘤治疗及预后判断。本文主要就microRNA在肿瘤发生发展和诊断中作用的研究进展进行了综述。     

MicroRNA-101 inhibits angiogenesis via COX-2 in endometrial carcinoma

Abnormal angiogenesis is critically involved in tumor progression and metastasis including endometrial cancer and is regulated by microRNAs such as microRNA-101 (miR-101). We hypothesize that miR-101 expression is disrupted in endometrial cancer and modulation of miR-101 levels is sufficient to regulate tumor growth through angiogenesis. We examined the expression levels of miR-101 and factors involved in angiogenesis in the patients with endometrial cancer. We also overexpressed or inhibited miR-101 in RL-95-2 cells and examined their effects on cell toxicity and tumor growth. Finally, we determined if miR-101 regulated tumorigenesis through cyclooxygenase-2 (COX-2). We found that miR-101 levels were significantly reduced. Factors involved in angiogenesis included vascular endothelial growth factor-A (VEGF-A), thrombospondin-1 (TSP-1), cyclooxygenase-2 (COX-2), prostaglandin E2 (PGE2), and aromatase (P450arom), which were increased in endometrial carcinoma. Modulation of miR-101 level was sufficient to affect tumor growth. Finally, we found that the effects of miR-101 inhibition on tumor growth were suppressed by COX-2 inhibition. Our results suggest that modulating miR-101 and COX-2 levels or their activity may be a potential therapeutic strategy for endometrial cancer.     

A microRNA component of the hypoxic response

microRNAs participate in a wide variety of physiological and pathological cellular processes. Recent studies have established a link between a specific group of microRNAs and hypoxia, a key feature of the neoplastic microenvironment. A significant proportion of the hypoxia-regulated microRNAs (HRMs) are also overexpressed in human cancers, suggesting a role in tumorigenesis. Preliminary evidence suggests that they could affect important processes such as apoptosis, proliferation and angiogenesis. Several HRMs exhibit induction in response to HIF activation, thus extending its repertoire of targets beyond translated genes. In the present review, we discuss the emerging roles of HRMs in oxygen deprivation in cancer context.     

Distinctive microRNA signature associated of neoplasms with the Wnt/β-catenin signaling pathway

As the crucial biological regulators, microRNAs that act by suppressing their target genes are involved in a variety of pathophysiological processes. It is generally accepted that microRNAs are often dysregulated in many types of neoplasm and other human diseases. In neoplasm, microRNAs may function as oncogenes or tumor suppressors. As constitutive activation of the Wnt signaling pathway is a common feature of neoplasm and contributes to its development, progression and metastasis in various cancers, numerous studies have revealed that microRNA-mediated gene regulation are interconnected with the Wnt/β-catenin signaling pathway, forming a Wnt/β-catenin–microRNA regulatory network, which is critical to successful targeting of the Wnt/β-catenin pathway for oncotherapy. In this review, we aim to accumulate recent advances on microRNAs that work in tandem with Wnt/β-catenin signaling in tumorigenesis, with particular focus on how microRNAs affect Wnt/β-catenin activity as well as how microRNAs are regulated through the Wnt/β-catenin pathway.     

Regulation of microRNA Expression: the Hypoxic Component

microRNAs are involved in a wide variety of normal and pathological cellular processes, including tumorigenic transformation. Despite significant progress made towards understanding their mechanisms of action, much less is known about the regulation of expression of specific microRNAs. Recent reports have established a link between hypoxia, a key feature of the tumor microenvironment, and a group of microRNAs. Select members of this group seem to affect apoptotic signaling in a hypoxic environment and are also predicted to target genes of critical importance for tumor biology. Interestingly, most hypoxia-induced microRNAs are also overexpressed in human cancers, suggesting a role in tumorigenesis. We hereby discuss the known and predicted regulators of microRNA expression and approaches for expanding this fledgling research area.     

MicroRNAs targeting prostate cancer stem cells

Prostate cancer is a frequently diagnosed cancer in males with high mortality in the world. As a heterogeneous tissue, the tumor mass contains a subpopulation that is called as cancer stem cells and displays stem-like properties such as self-renewal, epithelial–mesenchymal transition, metastasis, and drug resistance. Cancer stem cells have been identified in variant tumors and shown to be regulated by various molecules including microRNAs. MicroRNAs are a class of small non-coding RNAs, which can influence tumorigenesis via different mechanisms. In this review, we focus on the functions of microRNAs on regulating the stemness of prostate cancer stem cells with different mechanisms and propose the potential roles of microRNAs in prostate cancer therapy.     

Dysregulation of cellular microRNAs by human oncogenic viruses – Implications for tumorigenesis

Infection with certain animal and human viruses, often referred to as tumor viruses, induces oncogenic processes in their host. These viruses can induce tumorigenesis through direct and/or indirect mechanisms, and the regulation of microRNAs expression has been shown to play a key role in this process. Some human oncogenic viruses can express their own microRNAs; however, they all can dysregulate the expression of cellular microRNAs, facilitating their respective life cycles. The modulation of cellular microRNAs expression brings consequences to the host cells that may lead to malignant transformation, since microRNAs regulate the expression of genes involved in oncogenic pathways. This review focus on the mechanisms used by each human oncogenic virus to dysregulate the expression of cellular microRNAs, and their impact on tumorigenesis.     

miR-141 and miR-200a act on ovarian tumorigenesis by controlling oxidative stress response

Although there is evidence that redox regulation has an essential role in malignancies, its impact on tumor prognosis remains unclear. Here we show crosstalk between oxidative stress and the miR-200 family of microRNAs that affects tumorigenesis and chemosensitivity. miR-141 and miR-200a target p38α and modulate the oxidative stress response. Enhanced expression of these microRNAs mimics p38α deficiency and increases tumor growth in mouse models, but it also improves the response to chemotherapeutic agents. High-grade human ovarian adenocarcinomas that accumulate miR-200a have low concentrations of p38α and an associated oxidative stress signature. The miR200a-dependent stress signature correlates with improved survival of patients in response to treatment. Therefore, the role of miR-200a in stress could be a predictive marker for clinical outcome in ovarian cancer. In addition, although oxidative stress promotes tumor growth, it also sensitizes tumors to treatment, which could account for the limited success of antioxidants in clinical trials.