表观遗传学与肺癌

表观遗传学是指无DNA序列变化、可遗传的基因表达的改变.表观遗传学的分子机制主要包括DNA甲基化及组蛋白修饰,这些生物大分子的修饰在细胞周期,基因组印记、X染色体的失活中起重要作用.表观遗传学的改变与肿瘤及肺癌的发生、发展密切相关,它在疾病中的重要性越来越受到关注,表观遗传学的改变有可能成为新的诊断、监测及治疗的工具.     

表观遗传学与肺癌

表观遗传学是指无DNA序列变化、可遗传的基因表达的改变。表观遗传学的分子机制主要、N包括DNA甲基化及组蛋白修饰,这些生物大分子的修饰在细胞周期、基因组印记、x染色体的失活中起重要作用。表观遗传学的改变与肿瘤及肺癌的发生、发展密切相关,它在疾病中的重要性越来越受到关注,表观遗传学的改变有可能成为新的诊断、监测及治疗的工具。     

表观遗传学变化在胃癌诊断和预后中的应用

胃癌的恶性程度高且预后较差,目前随着对胃癌基础研究的不断深入,表观遗传学改变在胃癌发生发展中的重要作用逐渐被人们认识,特别是基因启动子区域的DNA甲基化被认为是肿瘤中普遍发生的分子改变,本文主要论述了胃癌相关基因甲基化状态的研究进展,目的在于探讨表观遗传学在胃癌早期诊断及预后中的意义。     

胃癌的表观遗传学研究

胃癌高度恶性且预后较差,目前随着对胃癌基础研究的不断深入,表观遗传学改变在胃癌发生发展中的重要作用逐渐被人们认识,因此可通过检测基因的异常甲基化等表观遗传学改变对胃癌进行早期诊断、治疗及预后评价。本文总结分析胃癌相关基因甲基化状态及表观遗传学的临床应用前景,以期探讨表观遗传学对胃癌的早期诊断及治疗的指导作用。     

表观遗传修饰与肿瘤

表观遗传学是指基因表达或蛋白表达的改变不涉及DNA序列变化,但又可以通过细胞分裂和增殖而稳定遗传的现象,主要包括基因组印记、DNA甲基化、组蛋白修饰和非编码RNA等。近年来,随着人们对表观遗传学认识的深入,尤其是去甲基化药物阿扎胞苷(azacitidine)及其脱氧衍生物5-氮杂2’-脱氧胞苷(5-Aza-dC)在治疗肿瘤患者的成功临床应用,表观遗传学逐渐成为肿瘤研究热点,本文就DNA甲基化和组蛋白修饰在肿瘤诊断及治疗等方面的研究作简要介绍。     

动脉粥样硬化的表观遗传学研究进展

动脉粥样硬化是环境因素与遗传因素相互作用所致的慢性炎症疾病.表观遗传修饰可能是链接环境因素与遗传因素的桥梁,深入了解表观遗传修饰如DNA甲基化、组蛋白修饰以及微小RNA对动脉粥样硬化形成和发展的影响及其作用机制,将进一步阐明动脉粥样硬化的发病机制.并且由于表观遗传修饰可逆,这可能为动脉粥样硬化的治疗提供新的策略和靶点.     

食管癌的表观遗传学特征

表观遗传学是一门研究基因表达的学科,经典的表观遗传学包括DNA甲基化和组蛋白修饰,microRNA对基因表达的调控也属于表观遗传学的范畴。食管癌发生过程中表观遗传学的改变已成为目前的研究热点,为食管癌的早期诊断、治疗和预后提供了新的手段。     

表观遗传学在胃癌中的应用价值

表观遗传学是一门研究基因表达的学科,其主要研究内容包括DNA甲基化、组蛋白修饰和非编码RNA。在胃癌的发生过程中表观遗传学的作用越来越受到人们的重视,特别是DNA甲基化改变的临床价值已被广泛接受。表观遗传学的变化不仅可用于胃癌的早期诊断,而且还可用作预后和化疗敏感性的指标。本文将对表观遗传学在胃癌中的应用价值进行较为系统的评价。     

食管癌表观遗传调控机制研究进展

近年来随着对肿瘤研究的深入,人们发现DNA序列以外的表观遗传调控异常在肿瘤的发生、发展过程中更为普遍、也更为重要。这种基于非基因序列改变所致基因表达水平变化的表观遗传学研究,包含了DNA甲基化、染色质组蛋白修饰、隔离蛋白及非编码RNA等调控方式。异常的表观遗传机制影响基因的转录,贯穿肿瘤发生、发展的整个过程,并具有一定的广泛性和组织特异性。食管癌是最常见的恶性肿瘤之一,开展食管癌表观遗传研究为其诊断、治疗和预防等方面提供了新思路。     

弓形虫表观遗传学研究进展

弓形虫复杂的生活史包含多个生命阶段、多种宿主和多种生存环境,从一个阶段向另一个阶段的转换,对外部环境的适应,均需要精密的基因表达调控机制。生物信息学分析表明,弓形虫缺乏其他真核生物典型的转录因子,却存在着丰富的表观遗传学机制。相关研究证明,弓形虫在转录后水平存在着以组蛋白修饰为主的大量修饰机制,如乙酰化、甲基化、磷酸化、泛素化和类泛素化等;同时发现弓形虫非编码RNA在弓形虫的基因表达调控中发挥了重要作用。这些结果为进一步揭示弓形虫的致病机制,从而有效防治弓形虫感染提供了可靠依据。     

表观遗传学在支气管哮喘发病机制中的研究进展

气道炎症与气道重塑是支气管哮喘(哮喘)长期反复发作以及病死率逐渐升高的主要原因。近年来,随着对表观遗传学认识的深入,人们逐步发现了表观遗传学在哮喘发生发展中的重要作用。本文综述了DNA甲基化、组蛋白修饰和microRNA基因调控三大表观遗传学在哮喘发病机制中的作用。     

Role of epigenetics in transformation of inflammation into colorectal cancer

Molecular mechanisms associated with inflammation-promoted tumorigenesis have become an important topic in cancer research. Various abnormal epigenetic changes, including DNA methylation, histone modification, chromatin remodeling, and noncoding RNA regulation, occur during the transformation of chronic inflammation into colorectal cancer(CRC). These changes not only accelerate transformation but also lead to cancer progression and metastasis by activating carcinogenic signaling pathways. The NF-κB and STAT3 signaling pathways play a particularly important role in the transformation of inflammation into CRC, and both are critical to cellular signal transduction and constantly activated in cancer by various abnormal changes including epigenetics. The NF-κB and STAT3 signals contribute to the microenvironment for tumorigenesis through secretion of a large number of pro-inflammatory cytokines and their crosstalk in the nucleus makes it even more difficult to treat CRC. Compared with gene mutation that is irreversible, epigenetic inheritance is reversible or can be altered by the intervention. Therefore, understanding the role of epigenetic inheritance in the inflammation-cancer transformation may elucidate the pathogenesis of CRC and promote the development of innovative drugs targeting transformation to prevent and treat this malignancy. This review summarizes the literature on the roles of epigenetic mechanisms in the occurrence and development of inflammation-induced CRC. Exploring the role of epigenetics in the transformation of inflammation into CRC may help stimulate futures studies on the role of molecular therapy in CRC.     

Celiac disease: From genetics to epigenetics

Celiac disease(CeD)is a multifactorial autoimmune disorder spread worldwide.The exposure to gluten,a protein found in cereals like wheat,barley and rye,is the main environmental factor involved in its pathogenesis.Even if the genetic predisposition represented by HLA-DQ2 or HLA-DQ8 haplotypes is widely recognised as mandatory for CeD development,it is not enough to explain the total predisposition for the disease.Furthermore,the onset of CeD comprehend a wide spectrum of symptoms,that often leads to a delay in CeD diagnosis.To overcome this deficiency and help detecting people with increased risk for CeD,also clarifying CeD traits linked to disease familiarity,different studies have tried to make light on other predisposing elements.These were in many cases genetic variants shared with other autoimmune diseases.Since inherited traits can be regulated by epigenetic modifications,also induced by environmental factors,the most recent studies focused on the potential involvement of epigenetics in CeD.Epigenetic factors can in fact modulate gene expression with many mechanisms,generating more or less stable changes in gene expression without affecting the DNA sequence.Here we analyze the different epigenetic modifications in CeD,in particular DNA methylation,histone modifications,non-coding RNAs and RNA methylation.Special attention is dedicated to the additional predispositions to CeD,the involvement of epigenetics in developing CeD complications,the pathogenic pathways modulated by epigenetic factors such as microRNAs and the potential use of epigenetic profiling as biomarker to discriminate different classes of patients.     

Epigenetic mechanisms in coronary artery disease: The current state and prospects

Coronary artery disease (CAD) is the leading cause of morbidity and mortality. CAD has both genetic and environmental causes. In the past two decades, the understanding of epigenetics has advanced swiftly and vigorously. It has been demonstrated that epigenetic modifications are associated with the onset and progression of CAD. This review aims to improve the understanding of the epigenetic mechanisms closely related to CAD and to provide a novel perspective on the onset and development of CAD. Epigenetic changes include DNA methylation, histone modification, microRNA and lncRNA, which are interrelated with critical genes and influence the expression of those genes. In addition, miRNA plays a diverse role in the pathological process of CAD. Numerous studies have found that some cardiac-specific miRNAs have potential as certain diagnostic biomarkers and treatment targets for CAD. In this review, the aberrant epigenetic mechanisms that contribute to CAD will be discussed. We will also provide novel insight into the epigenetic mechanisms that target CAD.     

组蛋白甲基化修饰在动脉粥样硬化发生发展中的研究进展

随着人们生活方式的改变,动脉粥样硬化的发病率逐年增长。目前,表观遗传学机制已成为动脉粥样硬化发病机制研究的新热点,组蛋白修饰作为一种重要的表观遗传调控机制得到了广泛的关注与研究。其中,组蛋白甲基化修饰是组蛋白修饰的重要形式之一,研究表明其与动脉粥样硬化的发生发展有着密不可分的联系。本文以几个重要的组蛋白甲基化修饰位点在动脉粥样硬化发生发展中的作用作为切入点,对这一领域的研究进展进行综述。     

表型遗传修饰对人结肠癌细胞周期和抑癌基因表达的调控

目的：分析和探讨同一结肠癌细胞系DNA甲基化和组蛋白乙酰化对抑癌基因表达和细胞周期的影响。方法：培养结肠癌细胞HT－29、SW1116和Colo-320，分别以去甲基化制剂5－氮脱氧胞苷（5－aza-dC）和（或）组蛋白脱乙酰化酶（HDAC）抑制剂trichostatinA(TSA)及丁酸盐干预细胞。提取基因组DNA和RNA，部分行甲基化特异性PCR（MSP）检测p16^INK4A基因启动子区甲基化情况；以RTPCR研究p16^INK4A和p^21WAF1 mRNA表达水平；同时以流式细胞仪分析SW1116和Colo-320细胞周期。结果：干预前，HT－29、SW1116和Colo-320三种结肠癌细胞系中均有较弱的p16^INK4A表达；SW1116和Colo-320细胞的p21^WAF1表达缺如，对于HT－29细胞，1μmol/L的5－aza-dC干预时则无显著改变。在SW1116和Colo-320细胞中，5－aza-dC干预后p16^INK4A表达增强，且以10μmol/L或5μmol/L浓度干预24h者为最明显，相反p21^WAF1仍无明显表达，该两个细胞系经TSA或丁酸盐使细胞阻滞于G1期。结论：三种人结肠癌细胞中，p16^INK4A基因的表达均受甲基化调节。SW1116和Colo-320细胞中p21^WAF1基因表达主要受乙酰化调节，在该两个细胞系中，乙酰化使细胞周期停滞于G1期。