MicroRNA 与胶质瘤的分子病理特征研究进展

MicroRNAs(miRNAs)是一类非编码的内源性小RNA分子,通过调节mRNA的稳定性及蛋白翻译过程控制基因表达,从而发挥促癌或抑癌作用;研究表明,在胶质瘤的发生、进展、侵袭过程中,伴随发生了许多分子病理特征的改变,这一过程中miRNAs发挥着重要作用,本文就此方面研究进展进行综述。     

miRNAs在肝癌干细胞中的作用

MicroRNAs (miRNAs)是一类参与转录后调控的小分子RNA,它在调控细胞的增殖、分化及肿瘤的形成等多种生理及病理过程中发挥着重要的作用.肝癌干细胞是肝癌组织中具有自我更新能力和分化潜能的一个微群体,它能够启始肝癌的发生,并且与肝癌的抗药性及复发等密切相关.已经有研究表明miRNAs对肝癌干细胞的发生发展起着重要的调控作用,包括致癌和抑癌的作用,因此总结miRNAs在肝癌干细胞中作用,有助于更好理解肝癌干细胞的特性及肝癌肿瘤生物学.近年来,除了传统的分子生物学手段,组学和系统生物学研究策略的运用也为miRNAs在肝癌中的研究提供了新的思路.鉴于此,深入研究miRNAs在肝癌干细胞中的分子机制,将为靶向肝癌干细胞的临床治疗提供新的途径.     

microRNA在心脏发育与疾病中功能研究进展

microRNAs(miRNAs)是一种基因组编码的小RNA,它们通过与目标mRNA分子的3'端非编码区域(3'UTR)互补配对导致mRNA分子稳定性和翻译受到抑制,在调节细胞增殖、凋亡、分化和肿瘤发生等多种生物学过程中起重要作用.心脏是人体的重要器官之一,其发育与疾病发生过程非常复杂,受到多种信号通路的调控.近期的研究表明,miRNAs在心脏的发生发育与疾病过程中都发挥着重要的作用,本文将对这方面的研究进展作一综述.     

microRNAs调节肿瘤细胞转移表型的分子机制

microRNAs(miRNAs)是一类在转录后水平调控基因表达的内源性非编码小RNA分子.miRNAs具有癌基因与抑癌基因的功能,参与肿瘤细胞的增殖、粘附、侵袭、转移和肿瘤血管形成等过程.miRNAs可调节肿瘤细胞转移表型,主要通过改变肿瘤细胞黏附力、侵袭力与迁移力.本文重点介绍调节肿瘤细胞转移表型相关miRNAs及其作用的分子机制,以便为肿瘤转移的研究提供新思路.     

miRNAs表达异常与卵巢癌发生发展的研究进展

微小RNAs(microRNAs,miRNAs)是一类长度约22 nt的内源性非编码RNAs,主要通过转录后沉默调控基因的表达,参与细胞增殖、分化、凋亡等重要病理生理过程以及某些肿瘤的发生发展与转移。miRNAs在卵巢癌细胞中存在广泛差异性表达,有望通过干扰miRNAs的生物发生(即放大miRNAs的抑癌作用或减弱miRNAs的致癌作用)达到预防和治疗卵巢癌的作用。该文对近年来miRNAs在卵巢癌发生发展中作用的研究结果进行综述,希望能为卵巢癌的临床治疗提供新思路。     

血小板囊泡microRNAs胞间传递与功能研究进展

人们对microRNAs(miRNAs)的研究已近二十年。从胞浆miRNAs到核miRNAs,再到胞外miRNAs,miRNAs的定位与作用机制越来越丰富。血小板不仅参与机体凝血过程,而且在机体免疫中也发挥重要作用。近年,人们发现血小板中富含miRNAs,并通过囊泡等"膜系统"向其周围细胞进行信息分子的传递,调控周围细胞的功能。对血小板囊泡miRNAs的认识,将有助于我们进一步理解血小板在凝血与免疫中的作用。     

微小RNAs在肝癌中的作用机制及相关应用研究进展

微小RNAs(miRNAs)是一类内源性小型非编码RNA,可通过调控靶基因表达参与大多数生物学过程。近年来,miRNAs在肝癌发生发展进程中相关作用机制的研究逐渐深入,miRNAs作为其中关键调控因子和主要参与者,已成为肝癌早期诊断、靶向治疗和预后评估中的一个关键靶标。本文着重强调miRNAs在肝癌发生发展、多重耐药性中的作用以及作为肝癌潜在治疗靶点的价值,并就miRNAs在肝癌中的功能、分子作用通路以及应用三方面的相关研究进展进行综述。     

MicroRNA与肺癌发生、诊断及治疗

微小RNA(miRNAs)是一大类小的非编码RNA,它通过与靶mRNA 3′非翻译区部分互补配对来调节特定基因的表达。近来研究表明,miRNA可作为癌基因或抑癌基因在肺癌发生发展过程中起重要作用。比较癌组织和非癌组织中miRNA表达谱的差异可筛选出部分miRNA分子作为肺癌诊断和预后判断的潜在生物标记。调节具有致癌或抑癌功能的miRNA表达可能成为肺癌治疗新方法,而结合传统放化疗及其敏感性miRNA标志也为肺癌治疗研究提供了新的策略。该文对miRNA在肺癌发生与发展、基因诊断和治疗中的作用做一综述。     

miRNAs表达异常在宫颈癌转移机制中的研究进展

原发宫颈癌(cervical cancer,CC)的早期转移是导致其治疗效果差的主要原因之一。因此,全面了解宫颈癌的转移机制至关重要。miRNAs(microRNAs)是一种小的非编码RNA分子,主要通过转录调控基因的表达,在肿瘤的发生发展过程中发挥重要的作用。miRNAs通过调节上皮–间质转化(epithelial-mesenchymal transition,EMT)、微血管的形成、细胞外基质(extracellular matrix,ECM)的降解及细胞骨架重构等多种途径影响宫颈癌的转移。该文就miRNAs在宫颈癌转移机制中的研究进展作一综述,以便为基于miRNAs开发抗宫颈癌转移的靶向药物提供参考依据。     

宿主-病毒在miRNA水平上的相互作用

微RNA(microRNA,miRNA)是近来发现的重要基因调节子,在许多生物学过程包括抗病毒防御中发挥着重要作用.越来越多的证据表明一些病毒或者编码它们自己的miRNAs或者颠覆细胞miRNAs.由此,宿主和病毒编码miRNAs及其靶标形成了宿主和病毒间新一调节层面的相互作用.深入理解宿主-病毒间miRNAs介导的相互作用,不仅有利于阐明病毒致病的分子基础,而且有利于制定更好的治疗策略.     

Classifying microRNAs in cancer: the good, the bad and the ugly

MicroRNAs (miRNAs) have quite recently emerged as a novel class of gene regulators. Many miRNAs exhibit altered expression levels in cancer, and we are only starting to understand the functional consequences of the loss or gain of particular miRNAs to the cancerous phenotype. miRNAs can be classified with regard to their role in cancer as the Good, the Bad and the Ugly. The "Good", those miRNAs that are innocent bystanders in the oncogenic transformation process, whose expression profile might even be used for cancer diagnosis or prognosis. The "Bad", those miRNAs that are causally linked to tumorigenesis and directly modify tumor suppressor- or oncogenic- pathways. And the "Ugly", those miRNAs whose inappropriate loss or gain destabilizes the cellular identity of a tumor, which indirectly results in enhanced phenotypic variability and progression of the tumor. Hereunder we will discuss the possible ways in which miRNAs can be relevant to cancer biology, and possible experimental strategies for elucidating the mechanisms involved.     

miR-451与人类肿瘤关系的研究进展

Micro RNAs(miRNA)是一类在转录后水平调控基因表达的小分子非编码RNAs,通过调节细胞的增殖、分化、凋亡使机体维一个动态平衡。近年来,大量研究表明许多miRNA可作为原癌基因或者抑癌基因参与肿瘤的发生、发展,进一步研究发现,通过检测和调控这些miRNA,可用于肿瘤的早期诊断和治疗。最近一系列研究发现miRNA-451(miR-451)在许多肿瘤中存在差异性表达,与这些肿瘤的发生、发展、治疗有着密切的联系。本文对人类肿瘤中miR-451表达、调控的相关研究做一综述,为miR-451在肿瘤的诊断、治疗及预后中的应用提供重要资料。     

CREB与其相关的非编码RNA在肿瘤发生发展中的作用

cAMP反应元件结合蛋白（cAMP responsive element binding protein, CREB）是亮氨酸拉链家族转录因子。新近研究发现,其在肿瘤组织中的表达显著高于癌旁,被认为是体内的原癌基因之一。非编码RNA（non-coding RNA, ncRNA）是生物体内不能翻译成蛋白质的RNA,主要包括微小RNA（microRNA, miRNA）和长链非编码RNA（long non-coding RNA, lncRNA）等,其异常表达与肿瘤的发生发展密切相关,是目前肿瘤研究的热点。研究表明,CREB与ncRNA之间存在互动效应,并且二者之间的相互作用影响肿瘤的发生发展,然而miRNA和lncRNA的作用机制却不相同。肿瘤细胞内高表达的CREB在影响下游靶基因表达时能够正调控miRNA,而对lncRNA则有促进和抑制两方面的作用。反之,肿瘤细胞中一些低表达的miRNA能促进CREB的表达;有趣的是,高表达的lncRNA能够促进CREB的表达和诱导其活性增强。在影响下游靶基因表达时miRNA仅仅发挥抑制作用,而lncRNA则分别具有促进和抑制作用。本文结合我们的系列报道和最新的研究结果,对ncRNA与CREB的互动效应及其与肿瘤的发生发展之间的关系作一综述。     

microRNAs: Key players in virus-associated hepatocellular carcinoma

Hepatocellular carcinoma (HCC) is known as one of the major health problems worldwide. Pathological analysis indicated that a variety of risk factors including genetical (i.e., alteration of tumor suppressors and oncogenes) and environmental factors (i.e., viruses) are involved in beginning and development of HCC. The understanding of these risk factors could guide scientists and clinicians to design effective therapeutic options in HCC treatment. Various viruses such as hepatitis B virus (HBV) and hepatitis C virus (HCV) via targeting several cellular and molecular pathways involved in HCC pathogenesis. Among various cellular and molecular targets, microRNAs (miRNAs) have appeared as key players in HCC progression. miRNAs are short noncoding RNAs which could play important roles as oncogenes or tumor suppressors in several malignancies such as HCC. Deregulation of many miRNAs (i.e., miR-222, miR-25, miR-92a, miR-1, let-7f, and miR-21) could be associated with different stages of HCC. Besides miRNAs, exosomes are other particles which are involved in HCC pathogenesis via targeting different cargos, such as DNAs, RNAs, miRNAs, and proteins. In this review, we summarize the current knowledge of the role of miRNAs and exosomes as important players in HCC pathogenesis. Moreover, we highlighted HCV- and HBV-related miRNAs which led to HCC progression.     

Role of TGF-β signaling regulatory microRNAs in the pathogenesis of colorectal cancer

Transforming growth factor β (TGF-β) modulates tumor progression by regulating cell proliferation, apoptosis, metastasis, angiogenesis, and drug resistance. Biological and pharmacological agonists/antagonists, the interplay between intracellular signaling pathways, and microRNAs (miRNAs) control the initiation and activation of the TGF-β signaling pathway. It has been proposed that the expression profiles of tumor suppressor and oncogenic TGF-β miRNAs may be used for the classification, diagnosis, and prognosis of human malignancies. Deregulated miRNAs and aberrant activation of TGF-β signaling are frequently found in human colorectal cancers (CRCs), but a little is known about their mechanisms of action in the development and progression of colorectal carcinoma. This review summarizes the current knowledge of the role of TGF-β signaling regulatory miRNAs in the pathogenesis of CRC for a better understanding and hence better management of this disease.     

Stromal-induced downregulation of miR-1247 promotes prostate cancer malignancy

Cancer progression is strictly dependent on the relationship between tumor cells and the surrounding stroma, which supports cancer malignancy promoting several crucial steps of tumor progression, including the execution of the epithelial to mesenchymal transition (EMT) associated with enhancement in cell invasion, resistance to both anoikis and chemotherapeutic treatments. Recently it has been highlighted the central role of microRNAs (miRNAs) as regulators of tumor progression. Notably, in several tumors a strong deregulation of miRNAs is observed, supporting proliferation, invasion, and metabolic reprogramming of tumor cells. Here we demonstrated that cancer-associated fibroblasts induce a downregulation of miR-1247 in prostate cancer (PCa) cells. We proved that miR-1247 repression is functional for the achievement of EMT and increased cell invasion as well as stemness traits. These phenomena contribute to promote the metastatic potential of PCa cells as demonstrated by increased lung colonization in in vivo experiments. Moreover, as a consequence of miR-1247 downregulation, we observed a correlated increased expression level of neuropilin-1, a miR-1247 target involved as a coreceptor in the epidermal growth factor receptor signaling. Taken together, our data highlight miR-1247 as a potential target for molecular therapies aimed to block the progression and diffusion of PCa.