MicroRNA与胃癌的关系

微小RNA(microRNA)是一类内源性、长度约为16～29 nt非编码小RNA,在细胞发育、增殖、分化、凋亡等方面都起了重要作用.通过与靶mRNA完全或不完全互补配对,引起mRNA的降解或翻译抑制,从而对基因转录后水平进行调控.microRNA既可作为促癌基因参与恶性肿瘤的发生和发育过程,又可作为抑瘤基因控制恶性肿...     

miRNA与肿瘤

microRNA又称miRNA，是真核生物细胞中固有的一类长度约为22个核苷酸且不编码蛋白的小分子RNA。miRNAs广泛参与动植物生命活动的调控，如生长发育、营养物质的代谢和激素的分泌等。近年的研究表明miRNA通过调控细胞增殖、凋亡和分化在肿瘤的发生和发展中起着重要的作用。研究miRNA与肿瘤的关系将为肿瘤的诊断和治疗提供新的思路。     

容积调控性氯离子通道与肿瘤

容积调控性氯通道在细胞的容积调节、增殖及凋亡等生理过程中发挥重要作用，其分子结构尚未确定。近年研究发现容积调控性氯通道与肿瘤细胞的增殖、侵袭、迁移、凋亡及多药耐药性等恶性生物学行为有关。随着研究深入，容积调控性氯通道将成为抗肿瘤治疗的新靶点。     

MicroRNA生物学功能及其在肿瘤中的作用机制

MicroRNA是新近发现的一类调控性小分子RNA,通过降解靶基因mRNA或者转录后抑制靶基因表达而发挥作用。目前的研究已经发现microRNA参与调控发育、细胞分化、细胞凋亡、细胞能量代谢等多种生理过程以及心血管疾病、神经系统疾病、糖尿病、肿瘤等多种病理过程。本文就microRNA的生物学功能及其在肿瘤发生、发展中的作用机制做一综述。     

MicroRNA与甲状腺癌发生、发展关系的研究进展

人微小RNA(microRNA, miRNA)是一类进化上高度保守、细胞内源性表达的单链非编码小分子 RNA,其通过“种子序列”与靶基因mRNA碱基互补配对,从而在转录后水平调控靶基因的表达。大量报道发现, miRNA参与早期胚胎发育及细胞的增殖、分化、凋亡等多种生物学过程,其异常表达可能与多种疾病的发生、发展密切相关。近年研究证实,甲状腺癌组织中存在miRNA的表达紊乱,该文现就miR-NA在甲状腺癌中的表达、调控及其在甲状腺癌发生、发展、转移过程中的作用及其机制进行综述。     

MicroRNA及其作用靶点单核苷酸多态性研究进展

microRNA（miRNA）是一类长约21～25个核苷酸的小分子非编码RNA,通过与靶基因mRNA分子3′端未翻译区域（3′-untranslated region,3′UTR）特异性结合,负性调控靶mRNA的翻译,是一类非常重要的转录后调控因子,不仅与正常的细胞增殖、分化、凋亡、应激、脂肪代谢、生长发育和心脏功能调控等密切相关,同时也与恶性肿瘤以及心血管疾病等疾病的发生发展密切相关。单核苷酸多态性（single nucleotide polymorphism,SNP）是导致药物反应性和疾病易感性个体和种族差异的重要原因之一。近来的研究发现,编码microRNA的基因及microRNA的靶基因结合位点也存在SNP,这些SNP?魅死嗉膊∫赘行院鸵┪锓从π愿鎏宀钜焯峁┝诵碌慕馐汀?     

MicroRNA与心血管重构

MicroRNA为短小(18～25个核苷酸组成)单链非编码RNAs,几乎参与所有疾病的病理生理过程.心血管重构是多种心血管疾病发生与发展的病理基础,而microRNA在心血管重构中起重要调控作用.在心肌性疾病中,microRNA通过多种机制影响心肌细胞肥大、凋亡和间质纤维化;在血管重构性疾病中,不同microRNA通过多条信号通路调节血管平滑肌细胞增殖和分泌.     

MicroRNA-494参与多种疾病发生发展的分子机制研究进展

正微小RNA(microRNA,miRNA,miR)是一种由20~22个核苷酸组成的内源性非编码小分子单链RNA,它可以在后转录水平通过以完全互补或不完全互补的形式与mRNA的3’UTR区结合调控细胞增殖、分化及凋亡等多个生理病理过程~([1])。其中,miR-494是一种来源于染色体14q32.31的miRNA~([2])。近年来的研究发现miR-494参与人体多个     

microRNA在肿瘤表观遗传学中的研究进展

microRNA(miRNA)是一类长约22nt的非编码小RNA,转录后水平调节基因的表达,在个体发育、细胞的增殖、凋亡、分化中发挥重要的作用。近年来研究发现,miRNA的表达异常与肿瘤的发生关系密切。新近研究发现,属于广义表观遗传范畴的miRNA,其自身的表达不仅受到DNA甲基化等表观遗传的调控,而且两者可能存在相互作用,参与肿瘤的发生、发展。microRNA在肿瘤表观遗传学的研究将为肿瘤的诊断、治疗和预防开辟了新的思路和方向。     

血管重塑机制研究进展

血管重塑是改善缺血性疾病治疗预后的瓶颈,包括血管壁细胞和细胞外基质结构和形态变化。血流动力学变化通过机械转导机制激活一系列血管生物化学信号,内皮细胞分泌血管活性物质和细胞因子,平滑肌细胞分泌生长因子,可激活多种信号转导途径,通过调控基因表达使血管发生增殖、凋亡、迁移、炎性反应,以及细胞外基质分泌、沉积与降解等变化。本文综述了细胞因子和细胞周期调控蛋白参与血管重塑的研究现状,以及microRNA在调控细胞表型转换、调控炎性反应和调控细胞增殖等方面参与血管重塑。     

GRIM-19的功能及与肿瘤的相关性

GRIM-19最初被认为定位于细胞核,后来发现在线粒体中也有表达。GRIM-19还是线粒体中NADH脱氢酶1复合物的基本亚单位,在线粒体Ⅰ型呼吸过程中至关重要。在病毒感染导致细胞癌变的过程中,GRIM-19很可能是病毒癌基因结合的靶点,目前认为,GRIM-19参与和细胞的增殖、凋亡的调控过程,其表达降低或位点突变可以导致细胞的异常增殖和恶性转化。在肿瘤的形成及凋亡抑制中发挥着重要的作用。     

反义c-myc对增强顺铂引起骨肉瘤细胞凋亡作用的实验研究

目的：通过反义基因治疗降低人骨肉瘤MG-63细胞c-myc的表达，并探讨顺铂对c-myc低表达的人骨肉瘤MG-63细胞凋亡作用的影响。 方法： 以腺病毒为载体，构建表达反义c-myc的重组腺病毒（Ad-Asc-myc），并在体外转染骨肉瘤MG-63细胞，降低MG-63细胞c-myc的表达，与不同浓度的顺铂作用后，采用MTT、蛋白免疫印迹（Western blot）、逆转录-聚合酶链反应（RT-PCR）、流式细胞仪（FCM）、透射电镜等检测顺铂对骨肉瘤MG-63细胞体外增殖抑制、凋亡相关基因的表达和凋亡作用。 结果： 构建的Ad-Asc-myc体外转染MG-63细胞48 h后，可明显降低c-Myc蛋白表达，并与浓度为2.0 mg/L的顺铂作用2 h后 ，对MG-63细胞的体外增殖抑制率可达38.0%；转染的细胞Bcl-2表达降低，Bax表达增加，而E2F-1的表达无变化；FCM、电镜等显示Ad-Asc-myc转染后可诱导骨肉瘤细胞凋亡，并增加顺铂对骨肉瘤细胞的凋亡作用。 结论： 降低c-myc表达能诱导骨肉瘤MG-63细胞凋亡并增加顺铂对MG-63细胞的促凋亡作用。     

DNA methylation and apoptosis

DNA methylation is an epigenetic phenomenon known to play an increasingly important role in the etiology of cancer. Changes in DNA methylation patterns particularly in the promoter region of genes either in the form of hypomethylation or hypermethylation can have profound effects on gene expression. Hypermethylation in the promoter region of genes is involved in down regulation of the gene expression. Studies from various cancers have revealed that DNA methylation affects genes involved in different cellular pathways including apoptosis. Apoptosis or programmed cell death plays a vital role in the maintenance of cellular homeostasis, i.e. a balance between cell proliferation and cell death. Cancer cells are known to harbor defects in apoptotic pathway and disruption of apoptosis is considered as an important factor aiding its evolution. Evidence from literature indicates that DNA methylation mediated down regulation of genes involved in apoptosis could be a significant mechanism through which tumor cells avoid apoptosis.     

Notch信号通路的研究现状

Notch信号通路是一条进化上十分保守的信号转导系统。Notch受体通过与配体的相互作用转导细胞信号,从而在细胞增殖、分化、凋亡中发挥重要的调控作用。Notch信号通路平衡细胞增殖、分化、凋亡的重要性提示其可能与肿瘤细胞的异常调控相关。近来研究发现,在许多肿瘤细胞系中存在notch基因的异常活化,且失控的Notch信号与肿瘤细胞的生长调控相关。文章综述了就新近有关Notch信号通路的生理功能及其对肿瘤细胞的调控作用。     

microRNA-182 inhibits the proliferation and invasion of human lung adenocarcinoma cells through its effect on human cortical actin-associated protein

Lung cancer is one of the main causes of cancer death worldwide. The cortactin gene, CTTN, may play a pivotal role in the proliferation and invasion of tumors. A microRNA (miR-182) was cloned and used to study the expression of CTTN and its regulatory effects on the proliferation and invasion of the lung cancer cell line, A549. Cortactin protein and CTTN mRNA expression decreased in A549 cells that were transfected with the miR-182 expression plasmid. A cell proliferation assay indicated that miR-182 expression affected cell cycle regulation and suppressed proliferation of lung cancer cells in vitro. In addition, xenograft experiments confirmed the suppression of tumor growth in vivo, which was due to the promotion of apoptosis. In conclusion, endogenous mature miR-182 expression may have an important role in the pathogenesis of lung cancer through its interference with the target gene CTTN by epigenetic modification.     

STC2 基因在乳腺癌中的表达及抑制其表达对癌细胞生物学特性的影响研究

目的:探讨斯钙素鄄2(STC2)基因在乳腺癌中的表达及抑制其表达对癌细胞增殖、周期及凋亡的影响。方法: RT鄄PCR 及Western blot 分别检测乳腺癌组织中STC2 基因的mRNA 及蛋白表达,并分析其与病理特征的关系;将STC2-siRNA 转染人乳腺癌MCF-7 细胞,另设空白对照组(Control)和阴性对照组(NC-siRNA),转染48 h 后,Western blot 检测各组细胞中 STC2、ki67、细胞周期素(cyclin D1)、活化的含半胱氨酸的天冬氨酸蛋白水解酶3(Cleaved caspase3)、Notch1、Hes1 蛋白表达; CCK8 检测细胞增殖;流式细胞仪检测细胞周期及凋亡。结果:STC2 基因在乳腺癌中的mRNA 及蛋白表达均显著高于癌旁组 织(P<0.05);STC2 基因表达与乳腺癌患者年龄、组织学分级及是否发生转移无关(P>0郾05),与病理分期、肿瘤大小相关(P< 0.05);NC-siRNA 组STC2 的蛋白表达与Control 组差异无统计学意义(P>0.05),STC2鄄siRNA 组STC2 的蛋白表达显著低于 Control 组(P<0.05);STC2鄄siRNA 组细胞存活率、S 期和G2/ M 细胞及ki67、cyclin D1、Notch1、Hes1 蛋白表达显著低于Control 组,细胞凋亡率、G0/ G1 期细胞及Cleaved caspase3 蛋白表达显著高于Control 组(P<0.05)。结论:STC2 基因在乳腺癌中高表 达,其表达与病理分期和肿瘤大小相关,抑制其表达可降低癌细胞的增殖,阻滞细胞于G1 期,并诱导细胞凋亡,其机制与下调 ki67、cyclin D1 和上调Cleaved caspase3 表达及下调Notch1 信号通路有关。     

MiRNA-429 suppresses the growth of gastric cancer cells in vitro

Micro-RNAs(miRNAs) have been found to be implicated in a very wide range of physiological processes.This study was aimed to investigate the regulation of miRNA-429(miR-429) in gastric cancer cells on cell proliferation and apoptosis.Quantitative PCR was employed to detect the expressions of miR-429 after eukaryotic expression plasmid of miR-429 and its inhibitor were transiently transfected into poorly differentiated human gastric can-cer cell line BGC823.The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide(MTT) reduction as-says were used to examine proliferation ability.Apoptosis was analyzed by flow cytometry after transfection.The results showed that 48 h after transfection,overexpression of miR-429 reached maximum efficiency.Compared with mock transfection,miR-429 inhibited tumor cell proliferation significantly(P < 0.05) at 48 h and 72 h.of Overexpression of miR-429 promoted tumor cell apoptosis when compared with mock transfected cells(P < 0.05).On the contrary,miR-429 inhibitor promoted tumor cell proliferation and inhibited apoptosis when compared with controls(P < 0.05).Our results suggested that miRNA-429 may serve as a tumor suppressor during tumorigenesis of gastric cancer and may be a potential gastric cancer therapeutic target.     

miR-101 suppresses tumor proliferation and migration,and induces apoptosis by targeting EZH2 in esophageal cancer cells

Aim: To investigate the role of miR-101 in the regulation of tumor proliferation, invasion, apoptosis and to its target gene in human ESCC. Methods: The expression level of miR-101 in Eca109 cell line was determined by real-time polymerase chain reaction (PCR). After transfected with miR-101 mimics and inhibitor, proliferation, migration and apoptosis in ESCC cell line (Eca109) were detected by MTT, cell wound healing assay and flow cytometry, respectively. The expression of EZH2 in Eca109 cell was examined by immunohistochemical staining. Results: We found that miR-101 was significantly down-regulated in ESCC cell than in matched normal esophageal epithelium cell. The expression level of miR-101 was inversely correlated to EZH2 protein expression in ESCC cell. In Eca109 cells, over-expression of miR-101 significantly inhibited the migration and invasion of ESCC cells, and promotes cell apoptosis. Conclusions: These findings suggest that decreased expression of miR-101 might promote metastasis of human ESCC by inducing accumulation of EZH2 protein.     

IL-2 signals through Sgk1 and inhibits proliferation and apoptosis in kidney cancer cells

The interleukin-2 is a cytokine that is essential for lymphocytic survival and function. Ectopic expression of the IL-2 receptor in epithelial tissues has been reported previously, although the functional significance of this expression is still being investigated. We provided novel structural and functional information on the expression of the IL-2 receptor in kidney cancer cells and in other normal and neoplastic human epithelial tissues. In A-498 kidney cancer cells, we showed that IL-2 binding to its own receptor triggers a signal transduction pathway leading to the inhibition of proliferation and apoptosis. We found that the inhibition of proliferation is associated with Erk1/2 dephosphorylation, whereas the survival signals appear to be mediated by Sgk1 activation. This investigation focuses on the IL-2 induced regulation of Sgk1 and describes a role of the IL-2 receptor and Sgk1 in the regulation of epithelial tumor cell death and survival.     

2-甲氧基雌二醇对骨肉瘤MG63细胞增殖和凋亡的影响及其机制研究

目的探讨2-甲氧基雌二醇(2-methoxyestradiol,2-ME)对骨肉瘤MG63细胞增殖和凋亡的影响及其分子机制。方法不同浓度(0、10、20、40μmol/L)的2-ME作用于肿瘤细胞后,通过显微镜观察细胞形态变化、MTT实验检测增殖抑制、流式细胞术检测细胞周期和凋亡、Western Blot和qRT-PCR实验检测相关分子表达情况。结果随着2-ME浓度的增加,细胞形态学观察显示肿瘤细胞数量逐渐减少、变形;MTT实验表明2-ME对肿瘤细胞增殖抑制作用逐渐增强;流式细胞术结果显示,2-ME能剂量依赖性的诱导肿瘤细胞凋亡,使肿瘤细胞周期阻滞在G_0/G_1期;Western Blot和qRT-PCR实验结果表明,细胞内Bcl-2、VEGF的表达逐渐下降,而Caspase-3的表达则逐渐升高。结论2-ME能抑制骨肉瘤MG63细胞增殖、诱导凋亡,其作用机制可能与Bcl-2、VEGF、Caspase-3相关。