黑素瘤的发展和进展已归因于独立或组合的遗传和表观遗传事件。就遗传改变而言,在理解黑色素瘤的发病机理方面取得了显着进展。然而,最近的研究揭示了表观遗传机制在基因表达调控中的复杂参与,包括甲基化,染色质修饰和重塑,以及非编码RNA的多种活性。基因甲基化和miRNAs在黑色素瘤中的作用已经得到了相对较好的研究,但其他研究表明,染色质状态和长链非编码RNA差异表达的变化可导致关键基因调控的改变。一起来看,它们影响相互影响的信号通路的功能,相交,并形成局部扰动干扰整个系统活动的网络。这里,我们关注的是表观遗传事件如何与这些途径交织在一起,并有助于黑素瘤的分子发病机制.
The development and progression of melanoma have been attributed to independent or combined genetic and epigenetic events. There has been remarkable progress in understanding melanoma pathogenesis in terms of genetic alterations. However, recent studies have revealed a complex involvement of epigenetic mechanisms in the regulation of gene expression, including methylation, chromatin modification and remodeling, and the diverse activities of non-coding RNAs. The roles of gene methylation and miRNAs have been relatively well studied in melanoma, but other studies have shown that changes in chromatin status and in the differential expression of long non-coding RNAs can lead to altered regulation of key genes. Taken together, they affect the functioning of signaling pathways that influence each other, intersect, and form networks in which local perturbations disturb the activity of the whole system. Here, we focus on how epigenetic events intertwine with these pathways and contribute to the molecular pathogenesis of melanoma.