共查询到17条相似文献，搜索用时 140 毫秒
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王孝恩 《潍坊教育学院学报》2004,17(2):19-21
DNA的甲基化及甲基化异常在人体发育和肿瘤的发生中起着至关重要的作用。文中主要综述了几十年来人们对 DNA甲基化异常与基因转录及肿瘤发生之间关系的研究进展 ,尤其是最近的研究突破。 相似文献
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肿瘤微环境主要由肿瘤细胞、肿瘤相关间质细胞及细胞外基质组成。肿瘤细胞通过多种方式调控肿瘤微环境中的间质细胞,诱导间质细胞分化并发挥促肿瘤的作用,从而为肿瘤的生长及转移创造一个适宜的环境。DNA甲基化异常是肿瘤的特点。目前关于肿瘤的甲基化调控机制已有大量报道,对于肿瘤细胞与微环境中间质细胞的相互作用机制也有了一些报道。然而,关于肿瘤细胞对微环境间质细胞的甲基化调控机制以及这种调控对肿瘤发生发展的影响并没有系统的论述。本综述总结了肿瘤细胞对微环境中间质细胞甲基化调控机制的最新研究进展,以及间质细胞发生的一些促肿瘤改变,从而全面阐释了肿瘤细胞和间质细胞间的相互作用,同时总结了肿瘤细胞对肿瘤微环境的表观遗传学调控,尤其是甲基化调控在肿瘤进展中发挥了重要的作用。干预肿瘤细胞对微环境中间质细胞的甲基化调节过程,可以发挥抗肿瘤的作用。 相似文献
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表观遗传学是研究没有DNA序列变化的可遗传的基因表达的改变。它主要通过DNA的甲基化、组蛋自修饰、染色质重塑和非编码RNA调控等方式控制基因表达。近年发现,一个等位基因被另外一个等位基因在转录水平上沉默的副突变现象可能包含有表观遗传性质的变化。遗传学和表观遗传学系统既相区别,又彼此影响,相辅相成,共同确保细胞的正常功能。 相似文献
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抑癌基因Rb与P53的研究进展 总被引：1，自引：0，他引：1
符碧 《海南师范学院学报》2001,14(2):96-98
Rb和453均为抑癌基因，Rb全长大约200kb，定位于人13号染色体的13p14.1，它所编码的104kD磷酸蛋白参与细胞周期的调控，调控细胞增值。而P53窒长16－20kb，定位于人17号染色体的17p13.1，它所编码的53kD磷酸蛋白可通过调控CIPI基因表达而调控细胞生长。在很多肿瘤中已发现Rb和P53基因的突变与缺失，揭示了这两种基因与肿瘤发生有密切关系。 相似文献
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DNA甲基化是表观遗传修饰的重要组成成分,是一种重要的基因表达调控机制。本文在介绍DNA甲基化的形成及其修饰方式的基础上论述了DNA甲基化的生物学功能。 相似文献
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DNA甲基化的影响因素及对基因表达的调控 总被引：1，自引：0，他引：1
DNA甲基化是一种由DNA甲基转移酶介导的主要表观遗传修饰方式,是调节基因组功能的重要途径。本文重点综述了影响DNA甲基化的主要因素以及DNA甲基化与基因表达调控的关系。 相似文献
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细胞凋亡是一种通过内源DNA内切酶的激活而发生的细胞自然死亡,是机体的一种正常生理机制。但在病理状态下异常的细胞凋亡又与肿瘤等系统疾病的发生发展有密切关系。Bcl-2及相关基因是一类细胞凋亡调控基因,它们分别有抑制细胞凋亡(Bcl-2,Bcl—Ⅺ)和促使细胞凋亡(Bax,Bcl—Ⅹ_s)两种作用。 相似文献
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Zhao JH Zhang JS Wang Y Wang RG Wu C Fan LJ Ren XL 《Journal of Zhejiang University. Science. B》2011,12(11):935-942
DNA methylation plays an important role in the epigenetic regulation of gene expression during plant growth, development,
and polyploidization. However, there is still no distinct evidence in tobacco regarding the distribution of the methylation
pattern and whether it contributes to qualitative characteristics. We studied the levels and patterns of methylation polymorphism
at CCGG sites in 48 accessions of allotetraploid flue-cured tobacco, Nicotiana tabacum, using a methylation-sensitive amplified polymorphism (MSAP) technique. The results showed that methylation existed at a
high level among tobacco accessions, among which 49.3% sites were methylated and 69.9% allelic sites were polymorphic. A cluster
analysis revealed distinct patterns of geography-specific groups. In addition, three polymorphic sites significantly related
to tobacco mosaic virus (TMV) resistance were explored. This suggests that tobacco breeders should pay more attention to epigenetic
traits. 相似文献
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Although epidemiological data provide evidence that early life experience plays a critical role in human development, the mechanism of how this works remains in question. Recent data from human and animal literature suggest that epigenetic changes, such as DNA methylation, are involved not only in cellular differentiation but also in the modulation of genome function in response to early life experience affecting gene function and the phenotype. Such modulations may serve as a mechanism for life‐long genome adaptation. These changes seem to be widely distributed across the genome and to involve central and peripheral systems. Examining the environmental circumstances associated with the onset and reversal of DNA methylation will be critical for understanding risk and resiliency. 相似文献
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Hong-xing Li Lei Xiao Cheng Wang Jia-li Gao Yong-gong Zhai 《Journal of Zhejiang University. Science. B》2010,11(10):784-791
It is generally agreed that adipocytes originate from mesenchymal stem cells in what can be divided into two processes: determination
and differentiation. In the past decade, many factors associated with epigenetic signals have been proved to be pivotal for
the appropriate timing of adipogenesis progression. A large number of coregulators at critical gene promoters set up specific
patterns of DNA methylation, histone acetylation and methylation, and nucleosome rearrangement, that act as an epigenetic
code to modulate the correct progress of adipocyte differentiation and adipogenesis during adipogenesis. In this review, we
focus on the functions and roles of epigenetic processes in preadipocyte differentiation and adipogenesis. 相似文献
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A Methylome‐Wide Association Study of Trajectories of Oppositional Defiant Behaviors and Biological Overlap With Attention Deficit Hyperactivity Disorder 
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下载免费PDF全文 Edward D. Barker Esther Walton Charlotte A.M. Cecil Richard Rowe Sara R. Jaffee Barbara Maughan Thomas G. O'Connor Argyris Stringaris Alan J. Meehan Wendy McArdle Caroline L. Relton Tom R. Gaunt 《Child development》2018,89(5):1839-1855
In 671 mother–child (49% male) pairs from an epidemiological birth cohort, we investigated (a) prospective associations between DNA methylation (at birth) and trajectories (ages 7–13) of oppositional defiant disorder (ODD), and the ODD subdimensions of irritable and headstrong; (b) common biological pathways, indexed by DNA methylation, between ODD trajectories and attention deficit hyperactivity disorder (ADHD); (c) genetic influence on DNA methylation; and (d) prenatal risk exposure associations. Methylome‐wide significant associations were identified for the ODD and headstrong, but not for irritable. Overlap analysis indicated biological correlates between ODD, headstrong, and ADHD. DNA methylation in ODD and headstrong was (to a degree) genetically influenced. DNA methylation associated with prenatal risk exposures of maternal anxiety (headstrong) and cigarette smoking (ODD and headstrong). 相似文献
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Meng-wen Zhang Xu Che Shu Zheng Lei Zheng 《Journal of Zhejiang University. Science. B》2017,18(5):365-372
The tumor microenvironment (TME) plays an important role in supporting cancer progression. The TME is composed of tumor cells, the surrounding tumor-associated stromal cells, and the extracellular matrix (ECM). Crosstalk between the TME components contributes to tumorigenesis. Recently, one of our studies showed that pancreatic ductal adenocarcinoma (PDAC) cells can induce DNA methylation in cancer-associated fibroblasts (CAFs), thereby modifying tumor-stromal interactions in the TME, and subsequently creating a TME that supports tumor growth. Here we summarize recent studies about how DNA methylation affects tumorigenesis through regulating tumorassociated stromal components including fibroblasts and immune cells. We also discuss the potential for targeting DNA methylation for the treatment of cancers. 相似文献
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Marilyn J. Essex W. Thomas Boyce Clyde Hertzman Lucia L. Lam Jeffrey M. Armstrong Sarah M. A. Neumann Michael S. Kobor 《Child development》2013,84(1):58-75
Fifteen‐year‐old adolescents (N = 109) in a longitudinal study of child development were recruited to examine differences in DNA methylation in relation to parent reports of adversity during the adolescents’ infancy and preschool periods. Microarray technology applied to 28,000 cytosine–guanine dinucleotide sites within DNA derived from buccal epithelial cells showed differential methylation among adolescents whose parents reported high levels of stress during their children’s early lives. Maternal stressors in infancy and paternal stressors in the preschool years were most strongly predictive of differential methylation, and the patterning of such epigenetic marks varied by children’s gender. To the authors’ knowledge, this is the first report of prospective associations between adversities in early childhood and the epigenetic conformation of adolescents’ genomic DNA. 相似文献
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为分析LPS刺激前后对RIPK2基因甲基化的影响,试验采用凝胶电泳、亚硫酸氢盐、双荧光素酶报告系统和qRT-PCR方法分析LPS刺激前后RIPK2基因的甲基化模式及甲基化相关试剂对鸡RIPK2启动子活性及表达水平影响。结果表明：LPS刺激后鸡RIPK2基因甲基化水平从53.8%下降至15.4%;5-氮杂胞苷显著性提高鸡RIPK2启动子活性,促进基因表达;而CpG甲基转移酶M. SssI显著性抑制鸡RIPK2启动子活性,抑制基因表达。研究结果对提高家禽免疫和控制过度性炎症反应具有十分重要的现实意义。 相似文献