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Search Results: 1 - 10 of 616 matches for " miR-186 "
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Curcumin Promoted the Apoptosis of Cisplain-resistant Human Lung Carcinoma Cells A549/DDP through Down-regulating miR-186*
Ni TANG,Jian ZHANG,Yongping DU
Chinese Journal of Lung Cancer , 2010,
Abstract: Background and objective Curcumin, a natural compound, is derived from the rthizom of Curcuma longa. In vitro and in vivo preclinical studies have shown its anti-inflammatory, antioxidant, anticancer activities and so on. miR-186*, which was found by microarray technology, was highly expressed in lung carcinoma cells A549/DDP. The aim of this study is to illustrate whether Curcumin could promote the apoptosis of A549/DDP cells through regulating the expression of miR-186*. Methods An oligonucleotide microarray chip was used to profile microRNA (miRNA) expressions in A549/DDP cells treated with and without Curcumin. The significantly differentially expressed miRNA, which was selected from microarray chip, validated by quantitative real-time PCR. Ultimately, the remarkably expressed miRNA modulated the apoptosis assaying by flow cytometry expriments and the survival rate was measured by MTT method. Results The microarray chip results demonstrated: Curcumin altered the expression level of miRNAs compared with untreated control in A549/DDP cell line, miR-186* was significantly down-regulated after Curcumin treatment, which confirmed by quantitative real-time PCR. Downregulation of miR-186* expression by curcumin elevated the apoptosis, and the survival rate of A549/DDP cells decreased; but up-regulation of miR-186* expression by transfection its mimics restrained the apoptosis, the survival rate of A549/DDP cells increased, which were assayed by flow cytometry expriments and MTT method. Conclusion Modulation of miRNAs expression may be an important mechanism underlying the biological roles of Curcumin.
MicroRNAs targeting Nicastrin regulate Aβ production and are affected by target site polymorphisms
Charlotte Delay,Véronique Dorval,Sébastien S. Hébert
Frontiers in Molecular Neuroscience , 2014, DOI: 10.3389/fnmol.2014.00067
Abstract: Despite the growing number of genome-wide association studies, the involvement of polymorphisms in microRNA target sites (polymiRTS) in Alzheimer’s disease (AD) remains poorly investigated. Recently, we have shown that AD-associated single-nucleotide polymorphisms (SNPs) present in the 3′ untranslated region (3′UTR) of amyloid precursor protein (APP) could directly affect miRNA function. In theory, loss of microRNA (miRNA) function could lead to risk for AD by increasing APP expression and Aβ peptide production. In this study, we tested the hypothesis that Nicastrin, a γ-secretase subunit involved in Aβ generation, could be regulated by miRNAs, and consequently affected by 3′UTR polymorphisms. Bioinformatic analysis identified 22 putative miRNA binding sites located in or near Nicastrin 3′UTR polymorphisms. From these miRNA candidates, six were previously shown to be expressed in human brain. We identified miR-24, miR-186, and miR-455 as regulators of Nicastrin expression, both in vitro and under physiological conditions in human cells, which resulted in altered Aβ secretion. Using luciferase-based assays, we further demonstrated that rs113810300 and rs141849450 SNPs affected miRNA-mediated repression of Nicastrin. Notably, rs141849450 completely abolished the miR-455-mediated repression of Nicastrin. Finally, the rs141849450 variant was identified in 1 out of 511 AD cases but not in 631 controls. These observations set the stage for future studies exploring the role of miRNAs and 3′UTR polymorphisms in AD.
Principles of miRNA-Target Regulation in Metazoan Models
Epaminondas Doxakis
International Journal of Molecular Sciences , 2013, DOI: 10.3390/ijms140816280
Abstract: MicroRNAs (miRs) are key post-transcriptional regulators that silence gene expression by direct base pairing to target sites of RNAs. They have a wide variety of tissue expression patterns and are differentially expressed during development and disease. Their activity and abundance is subject to various levels of control ranging from transcription and biogenesis to miR response elements on RNAs, target cellular levels and miR turnover. This review summarizes and discusses current knowledge on the regulation of miR activity and concludes with novel non-canonical functions that have recently emerged.
慢性髓细胞白血病患者骨髓单个核细胞miR-203、miR-451、miR-17表达及其临床意义
杨再林,叶枫,但国蓉,陈洁平,张勇,邹仲敏
第三军医大学学报 , 2014,
Abstract: 目的分析探讨miR-203、miR-451、miR-17在慢性髓细胞白血病(chronicmyeloidleukemia,CML)骨髓单个核细胞中表达水平的动态变化及在不同治疗方案后的表达差异,评价miR-203、miR-451、miR-17的表达水平在CML诊治中应用的可行性。方法收集2011年1月至2014年1月在西南医院经细胞形态学、免疫学、细胞遗传学及分子生物学(morphologie,immunophenotypie,cytogenetic,molecular,MICM)联合检测,由WHO造血组织和淋巴系统肿瘤分类的标准确诊为CML的患者98例及20例正常对照,采用实时定量PCR检测miR-203、miR-451、miR-17的表达水平,同步检测BCR-ABL融合基因的表达水平。结果①CML患者的miR-203表达水平明显低于对照组(P<0.05),且逐步多元回归分析显示miR-203与BCR-ABL融合基因表达水平呈负相关(r=-0.934,P<0.01);②CML患者的miR-451表达水平明显低于对照组(P<0.05),miR-451与BCR-ABL融合基因表达水平呈负相关(r=-0.917,P<0.01);③miR-17表达水平在CML-CP患者中上升,在CML-AP、BP患者中下调,差异有统计学意义(P<0.05);④3种miRNA表达水平均提示传统化疗组与TKI治疗组、造血干细胞移植组有统计学差异,而TKI治疗组与造血干细胞移植组无统计学差异。结论miR-203、miR-451、miR-17表达水平与BCR-ABL融合基因表达水平、CML疾病分期、治疗和预后评估等均有密切关系,有望成为CML新的生物学标志。
Involvement of miR-214 and miR-375 in Malignant Features of Non-Small-Cell Lung Cancer by Down-Regulating CADM1  [PDF]
Megumi Ishimura, Mika Sakurai-Yageta, Tomoko Maruyama, Tomoko Ando, Masashi Fukayama, Akiteru Goto, Yoshinori Murakami
Journal of Cancer Therapy (JCT) , 2012, DOI: 10.4236/jct.2012.324050
Abstract: A tumor suppressor gene, CADM1, encoding an immunoglobulin superfamily cell adhesion molecule, is inactivated in various cancers, including non-small-cell lung cancer (NSCLC). Although promoter methylation is one of the mechanisms to suppress CADM1 expression, about half of tumors lacking CADM1 expression do not show methylation of the gene promoter. We herein investigated the possible involvement of microRNA (miRNA) in the down-regulation of CADM1. Using computational algorithms, miR-214 and miR-375 were identified as candidate miRNAs targeting CADM1. A luciferase reporter assay demonstrated that miR-214 and miR-375 repressed the promoter activity through 3’-UTR of CADM1. Quantitative RT-PCR analysis demonstrated that miR-214 and miR-375 was highly expressed in 21 (62%) and 17 cases (50%) of 34 primary NSCLCs. Notably, increased expression of miR-214 was preferentially observed in tumors with advanced pathological stages and in those lacking CADM1 expression but were not associated with the promoter methylation, suggesting that miR-214-mediated silencing would be another mechanism to suppress CADM1 expression. On the other hand, introduction of miR-214 or miR-375 into NSCLC cells decreased CADM1 protein expression. Furthermore, overexpression of miR-214 enhanced anchorage-independent growth of NSCLC cells, A549, whereas transfection of miRNA inhibitor, miR-214 or miR-375, significantly suppressed the in vitro wound healing activity of HCC827 cells. These findings suggest that overexpression of miR-214 and miR-375 could participate in the malignant features of NSCLC through down-regulating CADM1 and would provide a potential target for the treatment of a subset of NSCLC.
miR-21 与胰腺癌
miR-21 and Pancreatic Cancer
 [PDF]

张莉娜, 张弘
World Journal of Cancer Research (WJCR) , 2013, DOI: 10.12677/WJCR.2013.31001
Abstract:

微小RNA(microRNA, miRNA)是一类内源性小分子单链RNA,在细胞增殖、分化、凋亡尤其是肿瘤发生发展等生理病理过程中发挥重要作用。miR-21 是研究最早也是较特殊的miRNA 之一,其在几乎所有的实体肿瘤包括胰腺癌中高表达。miR-21 通过作用于靶基因调控胰腺癌发生发发展,在胰腺癌细胞增殖、分化、迁移、侵袭以及肿瘤耐药性等起发面关键作用,有望成为胰腺癌诊断、治疗以及判断预后的潜在的生物标志物,有着潜在的临床应用价值。
MicroRNAs (miRNAs) are a class of single-stranded, evolutionary conserved, noncoding RNA molecules,which play important roles in various physiological or pathological processes, such as cell proliferation, differentiation,apoptosis, and especially tumorigenesis. All of them, miR-21 is one of the first studied and most special miRNAs as it is over expressed in nearly all of soil tumors. miR-21 has been shown to regulate the progression of pancreatic caner by targeting tumor suppressor or oncogenes, playing a key role in cell proliferation, differentiation, migration, invasion and drug resistance of pancreatic cancer. Therefore, miR-21 will possibly be a potential biomarker for diagnosis, therapy and prognosis of pancreatic cancer, showing potentially clinical value.

 

miR-222在胃癌中的表达分析及其靶基因FOS的鉴定
朱恩东,李娜,肖斌,黎伯胜,毛旭虎,邹全明
第三军医大学学报 , 2010,
Abstract: 目的分析miR-222在胃癌中的表达水平并鉴定miR-222的靶基因。方法选取第三军医大学新桥医院普外科10例患者的胃癌及远癌组织,匀浆法提取总RNA,用Real-timePCR法检测miR-222表达。利用miRNA靶基因预测数据库TargetScan,MICROCOSM及PicTar对miR-222的靶基因进行预测。化学合成包含有miR-222结合位点的靶基因3′非编码区(3′UTR)退火引物,插入荧光素酶报告载体pMIR-REPORT及绿色荧光蛋白(GFP)报告载体pMIR-GFP-REPORT,检测荧光素酶的活性变化及观察GFP表达量,并在蛋白水平用Westernblot检测miR-222对靶基因的抑制。结?果miR-222在70%(7/10)的胃癌组织样本中表达上调。生物信息学(TargetScan,MICROCOSM及PicTar3个miRNA靶基因预测数据库)分析可得在包括人类在内的不同物种中,FOS基因3′UTR区都有miR-222的保守结合种子序列。通过荧光素酶活性检测和GFP抑制试验可得miR-222在mRNA水平可以与FOS基因结合。Westernblot结果显示miR-222可以抑制c-fos蛋白表达。结论miR-222在胃癌样本中表达上调,证明FOS为miR-222的一个靶基因。
The Role of Myc and the miR-17~92 Cluster in Histone Deacetylase Inhibitor Induced Apoptosis of Solid Tumors  [PDF]
Dominique R. Talbert, Robert L. Wappel, Diarmuid M. Moran, Scott A. Shell, Sarah S. Bacus
Journal of Cancer Therapy (JCT) , 2013, DOI: 10.4236/jct.2013.44102
Abstract:

In recent years histone deacetylase inhibitors (HDACi’s) have emerged as promising therapeutics for cancer. While favorable responses to HDACi’s as single agents have been shown in several hematological malignancies, very little efficacy has been demonstrated in solid tumors. c-Myc (Myc), an oncoprotein commonly over-expressed in cancer, has been shown by several studies to play a critical role in HDACi-mediated cellular death. To expand upon these findings and determine the role that Myc plays in this process in solid tumors, we compared the effect of two HDAC inhibitors, SAHA and LAQ824, on the proliferation of solid tumor cell lines expressing high versus low levels of Myc. We found that cells expressing high levels of Myc were more sensitive to HDACi. In addition, there were significant differences in the type of response to HDACi treatment between the two cell types with prominent apoptosis in cells expressing higher levels of Myc while cell cycle arrest was more commonly observed in cells expressing lower levels of Myc. Interestingly, HDACi reduced the expression of Myc and one of its well-known oncogenic miRNA targets, miR-17~92 cluster, resulting in an increase in the expression of the master pro-apoptotic protein Bim. We propose that this novel mechanism may play a role in the potent anti-proliferative effects mediated by HDACi. Furthermore, these studies suggest that Myc expression could be used as a predictive biomarker to select patients with solid tumors who may be more responsive to HDACi treatment.

Prognostic Role of miR-205 in Early-Stage (T1N0) Non-Small Cell Lung Cancer  [PDF]
Laura Boldrini, Mirella Giordano, Adele Servadio, Greta Alì, Alice Cocco, Marco Lucchi, Pietro Bertoglio, Franca Melfi, Alfredo Mussi, Gabriella Fontanini
Advances in Lung Cancer (ALC) , 2014, DOI: 10.4236/alc.2014.32007
Abstract:

Background: Published data have shown that microRNAs (miRNAs) could play a potential role as diagnostic and prognostic indicators in cancers. Data for the predictive value of miRNA let-7, miR-21, and miR-205 are inconclusive. The aim of the present analysis was therefore to evaluate the expression and the prognostic role of the above mentioned miRNAs in early-stage (T1N0) NSCLC patients. Methods: Quantification of let-7g, miR-21, and miR-205 expression was carried out into 105 early-stage NSCLC by quantitative Real Time-PCR (qRT-PCR). Results: a significant association between the low miR-205 expression and ADC histotype (p < 0.0001) compared to SCC was found; moreover, survival analysis showed thattumors with a high miR-205 expression had a significantly shorter mean PFS and OS compared to the patients with a low expression of this miRNA (p = 0.02 and p = 0.03, respectively). No other statistically significant correlations were observed between the analysed miRNAs and the main clinico-pathological characteristics of the NSCLC patients. Conclusion: The results indicated that miR-205 could represent a useful marker in the prognostic management of

MicroRNA-22E Inhibits HER-3 Protein Expression to Facilitate Metastasis of Lung Adenocarcinomas  [PDF]
Hsin-Yuan Fang, Tze-Yi Lin, Shiow-Her Chiou, Liang-Shun Wang, Kuan-Chih Chow
Journal of Cancer Therapy (JCT) , 2015, DOI: 10.4236/jct.2015.64039
Abstract:

MicroRNA-22 (miR-22), a short non-coding RNA that post-transcriptionally regulates mRNA stability and protein synthesis, has been shown to enhance metastatic potential and to suppress HER-3, an important mRNA marker for non-small cell lung cancer (NSCLC). However, the effect of miR-22 has not been investigated in lung adenocarcinoma (LADC), the most common type of NSCLC in the Far East. In this study, we analyzed the role of miR-22 expression in LADC patients. Expression of miR-22 was detected by reverse-transcription polymerase chain reaction (RT-PCR), and confirmed by cDNA sequencing. Signals of miR-22 in LADC sections were identified using in situ hybridization (ISH). The association between miR-22 expression and survival was evaluated by the log-rank test. Induction of miR-22 expression and the effect on HER-3 levels, as well as the subsequent cell behavior were also investigated In vitro. Two types of miR-22: miR-22 and miR-22H, were detected by RT-PCR. The miR-22H had extra 13 bases, 5’-TGTGTTCAGTGGT-3’, at the 3’-end, and this segment was named miR-22E. Using ISH, miR-22E overexpression was detected in 225 (83.0%) of 271 LADC patients. A significant difference was found in cumulative survival between patients with high miR-22E levels and those with low miR-22E levels (p < 0.0001). In vitro, epidermal growth factor induced miR-22, but reduced HER-3 expression. Expression of miR-22 increased cell movement ability. In conclusion, expression of miR-22 is closely associated with tumor recurrence, metastasis and overall survival in LADC patients by suppressing HER-3 protein expression to enhance epithelial-mesenchymal transition and metastasis.

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