Microdissecting the role of microRNAs in the pathogenesis of prostate cancer

被引:29
作者
Ayub, Shiekh Gazalla [1 ]
Kaul, Deepak [1 ]
Ayub, Taha [2 ]
机构
[1] Postgrad Inst Med Sci & Res, Dept Expt Med & Biotechnol, Chandigarh, India
[2] Govt Med Coll, Dept Social & Prevent Med, Srinagar, Jammu & Kashmir, India
关键词
miRNAs; PCa; androgen-dependent; androgen-independent; hormone-sensitive; castration-resistant; EPITHELIAL-MESENCHYMAL TRANSITION; ATTENUATES PACLITAXEL-RESISTANCE; ANDROGEN RECEPTOR EXPRESSION; GROWTH-FACTOR RECEPTOR; CARCINOMA-CELL LINES; TUMOR-SUPPRESSOR; DOWN-REGULATION; STEM-CELLS; PC3; CELLS; ENFORCED EXPRESSION;
D O I
10.1016/j.cancergen.2015.02.010
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
MicroRNAs (miRNAs) are naturally occurring, small, non-coding RNA molecules that post-transcriptionally regulate the expression of a large number of genes involved in various biological processes, either through mRNA degradation or through translation inhibition. Since the discovery of miRNAs, a vast amount of research has implicated the deregulated expression of miRNAs in different malignancies, including prostate cancer (PCa). Different miRNA expression profiles are reportedly associated with the development, progression, and emergence of castration-resistant PCa (CRPC), suggesting their use in the diagnosis, prognosis, and development of anti-cancer treatment models directed against this disease. However, before their exploitation in terms of therapeutics, a thorough understanding and in-depth mechanistic studies of these miRNAs and the gene networks they orchestrate are necessary for ascertaining their definitive role in the development and progression of PCa. This review attempts to extensively summarize the current knowledge of aberrantly expressed miRNAs and their mode of action in PCa, while highlighting the existing discrepancies and future research warranted.
引用
收藏
页码:289 / 302
页数:14
相关论文
共 150 条
[1]   Wnt proteins prevent apoptosis of both uncommitted osteoblast progenitors and differentiated osteoblasts by β-catenin-dependent and -independent signaling cascades involving Src/ERK and phosphatidylinositol 3-kinase/AKT [J].
Almeida, M ;
Han, L ;
Bellido, T ;
Manolagas, SC ;
Kousteni, S .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2005, 280 (50) :41342-41351
[2]   Genomic profiling of MicroRNA and messenger RNA reveals deregulated MicroRNA expression in prostate cancer [J].
Ambs, Stefan ;
Prueitt, Robyn L. ;
Yi, Ming ;
Hudson, Robert S. ;
Howe, Tiffany M. ;
Petrocca, Fabio ;
Wallace, Tiffany A. ;
Liu, Chang-Gong ;
Volinia, Stefano ;
Calin, George A. ;
Yfantis, Harris G. ;
Stephens, Robert M. ;
Croce, Carlo M. .
CANCER RESEARCH, 2008, 68 (15) :6162-6170
[3]   miR-15a and miR-16-1 in cancer: discovery, function and future perspectives [J].
Aqeilan, R. I. ;
Calin, G. A. ;
Croce, C. M. .
CELL DEATH AND DIFFERENTIATION, 2010, 17 (02) :215-220
[4]   Cross-talk unfolded:: MARCKS proteins [J].
Arbuzova, A ;
Schmitz, AAP ;
Vergères, G .
BIOCHEMICAL JOURNAL, 2002, 362 :1-12
[5]   New Strategies in Metastatic Prostate Cancer: Targeting the Androgen Receptor Signaling Pathway [J].
Attard, Gerhardt ;
Richards, Juliet ;
de Bono, Johann S. .
CLINICAL CANCER RESEARCH, 2011, 17 (07) :1649-1657
[6]   The quest for the 1p36 tumor suppressor [J].
Bagchi, Anindya ;
Mills, Alea A. .
CANCER RESEARCH, 2008, 68 (08) :2551-2556
[7]   Biochemical relapse following radical prostatectomy and miR-200a levels in prostate cancer [J].
Barron, Niall ;
Keenan, Joanne ;
Gammell, Patrick ;
Martinez, Vanesa G. ;
Freeman, Alex ;
Masters, John R. ;
Clynes, Martin .
PROSTATE, 2012, 72 (11) :1193-1199
[8]   MicroRNAs: Genomics, biogenesis, mechanism, and function (Reprinted from Cell, vol 116, pg 281-297, 2004) [J].
Bartel, David P. .
CELL, 2007, 131 (04) :11-29
[9]  
Barton BE, 2004, MOL CANCER THER, V3, P11
[10]   MYC Is Activated by USP2a-Mediated Modulation of MicroRNAs in Prostate Cancer [J].
Benassi, Barbara ;
Flavin, Richard ;
Marchionni, Luigi ;
Zanata, Silvio ;
Pan, Yunfeng ;
Chowdhury, Dipanjan ;
Marani, Marina ;
Strano, Sabrina ;
Muti, Paola ;
Blandino, Giovanni ;
Loda, Massimo .
CANCER DISCOVERY, 2012, 2 (03) :236-247