非编码RNA

缩写ncRNA,是指各种不翻译成蛋白质的RNA分子。其中包括rRNA,tRNA,snRNA,snoRNA 和microRNA 等多种已知功能的 RNA,还包括未知功能的RNA。

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首页 » 非编码RNA » 2017(第五届)非编码RNA研讨会嘉宾演讲摘要抢先预览

2017(第五届)非编码RNA研讨会嘉宾演讲摘要抢先预览

来源:生物谷 2017-09-28 16:36



 
生物谷于10月27日-28日在上海好望角大酒店(上海市徐汇区肇嘉浜路500号)举办2017第五届非编码RNA研讨会,此次会议将继续围绕非编码RNA调控机理,技术方法以及与疾病关系邀请国内外知名专家学者座谈,分享最新非编码RNA研究成果与经验,推动学科发展,促进转化医学及合作。

以下为本次大会演讲嘉宾及摘要内容,敬请预览>>

一、嘉宾演讲摘要

【卜鹏程】中国科学院生物物理研究所

演讲题目:非编码RNA对肠干细胞命运的调节及机制

 
干细胞可以进行不对称分裂,生成一个干细胞和一个分化的细胞。之前大家的研究集中理解蛋白质的不对称分布如何决定干细胞的命运, 我们近期的研究发现非编码RNA, miR-34a在肠癌干细胞分裂中不对称分布,调控干细胞的自我更新或分化。miR-34a在分化的细胞中高表达,干细胞中低表达。调节miR-34a的表达水平能够有效的调控肠癌干细胞的命运以及肠癌的发生和发展。miR-34a的不对称分布被一个长链非编码RNA, lnc34a调节。Lnc34a表达于miR-34a的启动子区,通过招募Dnmt3a和HDAC1抑制miR-34a在肠干细胞的表达。此外,miR-34a能够调控正常肠干细胞的不对称分裂。miR-34a介导的干细胞不对称分裂能够保护肠细胞在炎症条件下的恶性转化。炎症条件下,肠干细胞趋于快速扩增以修复炎症对上皮细胞的破坏。miR-34a介导的肠干细胞不对称分裂来控制干细胞有限扩增。miR-34a敲除后,肠干细胞转变为干细胞/干细胞对称分裂,干细胞趋于无限扩增并恶性转化...
 
【李家立】中国科学院昆明动物研究所

演讲题目:Annotation and cluster analysis of spatiotemporal- and sex-related lncRNA expression in Rhesus Macaque brain

 
Long noncoding RNA (lncRNA)-mediated epigenetic regulation plays important roles in wide range of biological processes and diseases. Here, we applied comprehensive analyses of RNA-seq and CAGE-seq (cap analysis of gene expression and sequencing) to characterize dynamic changes in lncRNA expression in rhesus macaque brain in four age groups from postnatal to aged periods. We identified 18 anatomically diverse lncRNA modules and 14 mRNA modules representing spatial, age and sex specificities. Spatiotemporal- and sex-biased changes in lncRNA expression are in general higher than that observed in mRNA expression. A negative correlation between lncRNA and mRNA expression in cerebral cortex was observed, such relationship was further explored and functionally validated. Our findings offer an initial insight into spatial-, age- and sex-biased changes in lncRNA expression in macaque brain, and that the distinct classification of such changes might represent a previously unappreciated regulatory system which potentially contributes to postnatal brain development and ageing....
 
【胡继繁】吉林大学第一医院肿瘤中心

演讲题目: FLI1 exonic circular RNAs promote tumor metastasis by coordinately regulating TET1 and DNMT1

Friend leukemia virus integration 1 (FLI1), an ETS transcription factor family member, acts as an oncogenic driver in hematological malignancies as well as in solid tumors. Immunohistochemical staining shows that FLI1 is aberrantly overexpressed in advanced stage and metastatic cancers. However, little is known about the factors that activate this proto-oncogene in tumors. Using “chromatin-lncRNA in situ reverse transcription trap sequencing” (CLIST-Seq), we have identified two circular RNA in the FLI1 promoter chromatin complex, consisting of FLI1 exons 4-2-3 and exons 5-2-3-4, referred to as circFLI1s.
CircFLI1s are located both in the cytoplasm and in the nucleus. Silencing of circFLI1s, but not the FLI1 linear mRNA, significantly inhibits the migration of two highly aggressive SCLC cell lines (NCI-H446 and NCI-H1688). Overexpression of circFLI1s enhances invasiveness of cancer cells. In a xenograft tumor model, downregulation of circFLI1s prolongs tumor survival and reduces the metastasis of tumors to the lung and the liver. Notably, we demonstrate that the nuclear circFLI1s utilize a positive feedback mechanism to activate FLI1 by inducing DNA demethylation in CpG islands of the promoter. Mechanistically, circFLI1s bind to the FLI1 promoter in cis and recruit TET1, a demethylase that is actively involved in DNA demethylation. CircFLI1s also bind to and downregulate in trans DNMT1, a methyltransferase that is essential for the maintenance of DNA methylation. Thus, nuclear circFLI1s act as an upstream regulator to control tumor growth by coordinating the regulation of DNA methylating and demethylating enzymes.
The cytoplasmic circFLI1s, however, act as a molecular sponge to sequester and consequently inactivate tumor suppressor microRNA miR584-3p. Rho Associated Coiled-Coil Containing Protein Kinase 1 (ROCK1), a downstream target of the microRNA, is inactivated by circFLI1 knockdown, but is upregulated by ectopic expression of circFLI1s. Thus, both the cytoplasmic and nuclear circFLI1s utilize distinct mechanisms to promote tumor growth. Clearly, FLI1 drives tumor metastasis not only through the canonical oncoprotein pathway, but also using epigenetic mechanisms mediated by its exonic circular RNA...
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四、联系方式

参会和媒体合作:
何春幸
E-mail: chunxing.he@medsci.cn
Mt: 17321087523 微信号medscihuiyi01
 
赞助和大会咨询:
胡睿
E-mail: rui.hu@bioon.com
Mt: 13636312725


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