Insights into the miRNA regulations in human disease genes

被引:32
作者
Das, Jyotirmoy [1 ]
Podder, Soumita [1 ]
Ghosh, Tapash Chandra [1 ]
机构
[1] Bose Inst, Bioinformat Ctr, Kolkata 700054, India
关键词
MicroRNAs; Cancer; mRNA decay rates; AREScores; Epigenetic modifications; UCSC GENOME BROWSER; MICRORNA; EPIGENETICS; DATABASE; CANCER; TARGETS;
D O I
10.1186/1471-2164-15-1010
中图分类号
Q81 [生物工程学(生物技术)]; Q93 [微生物学];
学科分类号
071005 ; 0836 ; 090102 ; 100705 ;
摘要
Background: MicroRNAs are a class of short non-coding RNAs derived from either cellular or viral transcripts that act post-transcriptionally to regulate mRNA stability and translation. In recent days, increasing numbers of miRNAs have been shown to be involved in the development and progression of a variety of diseases. We, therefore, intend to enumerate miRNA targets in several known disease classes to explore the degree of miRNA regulations on them which is unexplored till date. Results: Here, we noticed that miRNA hits in cancer genes are remarkably higher than other diseases in human. Our observation suggests that UTRs and the transcript length of cancer related genes have a significant contribution in higher susceptibility to miRNA regulation. Moreover, gene duplication, mRNA stability, AREScores and evolutionary rate were likely to have implications for more miRNA targeting on cancer genes. Consequently, the regression analysis have confirmed that the AREScores plays most important role in detecting miRNA targets on disease genes. Interestingly, we observed that epigenetic modifications like CpG methylation and histone modification are less effective than miRNA regulations in controlling the gene expression of cancer genes. Conclusions: The intrinsic properties of cancer genes studied here, for higher miRNA targeting will enhance the knowledge on cancer gene regulation.
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页数:7
相关论文
共 34 条
[21]   Conserved seed pairing, often flanked by adenosines, indicates that thousands of human genes are microRNA targets [J].
Lewis, BP ;
Burge, CB ;
Bartel, DP .
CELL, 2005, 120 (01) :15-20
[22]   An Analysis of Human MicroRNA and Disease Associations [J].
Lu, Ming ;
Zhang, Qipeng ;
Deng, Min ;
Miao, Jing ;
Guo, Yanhong ;
Gao, Wei ;
Cui, Qinghua .
PLOS ONE, 2008, 3 (10)
[23]   The elements of statistical learning: Data mining, inference and prediction. [J].
Marcoulides, GA .
STRUCTURAL EQUATION MODELING-A MULTIDISCIPLINARY JOURNAL, 2004, 11 (01) :150-151
[24]   Comparative analysis of the structural and expressional parameters of microRNA target genes [J].
Mok, Young-Joon ;
Park, Seung Gu ;
Choi, Sun Shim .
GENE, 2012, 497 (01) :103-109
[25]   The Contribution of RNA Decay Quantitative Trait Loci to Inter-Individual Variation in Steady-State Gene Expression Levels [J].
Pai, Athma A. ;
Cain, Carolyn E. ;
Mizrahi-Man, Orna ;
De Leon, Sherryl ;
Lewellen, Noah ;
Veyrieras, Jean-Baptiste ;
Degner, Jacob F. ;
Gaffney, Daniel J. ;
Pickrell, Joseph K. ;
Stephens, Matthew ;
Pritchard, Jonathan K. ;
Gilad, Yoav .
PLOS GENETICS, 2012, 8 (10)
[26]   MicroRNAs and epigenetics [J].
Sato, Fumiaki ;
Tsuchiya, Soken ;
Meltzer, Stephen J. ;
Shimizu, Kazuharu .
FEBS JOURNAL, 2011, 278 (10) :1598-1609
[27]   Genome-Wide Assessment of AU-Rich Elements by the AREScore Algorithm [J].
Spasic, Milan ;
Friedel, Caroline C. ;
Schott, Johanna ;
Kreth, Jochen ;
Leppek, Kathrin ;
Hofmann, Sarah ;
Ozgur, Sevim ;
Stoecklin, Georg .
PLOS GENETICS, 2012, 8 (01)
[28]   Evolutionary dynamics of oncogenes and tumor suppressor genes: Higher intensities of purifying selection than other genes [J].
Thomas, MA ;
Weston, B ;
Joseph, M ;
Wu, WH ;
Nekrutenko, A ;
Tonellato, PJ .
MOLECULAR BIOLOGY AND EVOLUTION, 2003, 20 (06) :964-968
[29]  
Valencia-Sanchez M, 2006, GENES DEV
[30]   TarBase 6.0: capturing the exponential growth of miRNA targets with experimental support [J].
Vergoulis, Thanasis ;
Vlachos, Ioannis S. ;
Alexiou, Panagiotis ;
Georgakilas, George ;
Maragkakis, Manolis ;
Reczko, Martin ;
Gerangelos, Stefanos ;
Koziris, Nectarios ;
Dalamagas, Theodore ;
Hatzigeorgiou, Artemis G. .
NUCLEIC ACIDS RESEARCH, 2012, 40 (D1) :D222-D229