Kent O A, Mendell J T
The McKusick-Nathans Institute of Genetic Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Oncogene. 2006 Oct 9;25(46):6188-96. doi: 10.1038/sj.onc.1209913.
The known classes of genes that function as tumor suppressors and oncogenes have recently been expanded to include the microRNA (miRNA) family of regulatory molecules. miRNAs negatively regulate the stability and translation of target messenger RNAs (mRNA) and have been implicated in diverse processes such as cellular differentiation, cell-cycle control and apoptosis. Examination of tumor-specific miRNA expression profiles has revealed widespread dysregulation of these molecules in diverse cancers. Although studies addressing their role in cancer pathogenesis are at an early stage, it is apparent that loss- or gain-of-function of specific miRNAs contributes to cellular transformation and tumorigenesis. The available evidence clearly demonstrates that these molecules are intertwined with cellular pathways regulated by classical oncogenes and tumor suppressors such as MYC, RAS and p53. Incorporation of miRNA regulation into current models of molecular cancer pathogenesis will be essential to achieve a complete understanding of this group of diseases.
已知发挥肿瘤抑制基因和癌基因功能的基因类别最近已扩展至包括调控分子的微小RNA（miRNA）家族。miRNA对靶信使核糖核酸（mRNA）的稳定性和翻译起负调控作用，并涉及多种过程，如细胞分化、细胞周期控制和细胞凋亡。对肿瘤特异性miRNA表达谱的研究揭示了这些分子在多种癌症中普遍失调。尽管关于它们在癌症发病机制中作用的研究尚处于早期阶段，但显然特定miRNA的功能丧失或获得会导致细胞转化和肿瘤发生。现有证据清楚地表明，这些分子与由经典癌基因和肿瘤抑制基因（如MYC、RAS和p53）调控的细胞通路相互交织。将miRNA调控纳入当前分子癌症发病机制模型对于全面理解这类疾病至关重要。
