Almost all genes in normal cells undergo alternative RNA splicing to generate a greater extent of diversification of gene products for normal cellular functions. RNA splicing is tightly regulated and closely interplays with genetic and epigenetic machinery. While DNA polymorphism and somatic mutations modulate alternative splicing patterns, RNA splicing also controls genomic stability, chromatin organization, and transcriptome. Tumor cells, in turn, often take advantage of aberrant RNA splicing to develop, grow and progress into therapy-resistant tumors. Understanding alternative RNA splicing in tumor cells would, therefore, provide us opportunities to gain further insights into tumor biology, identify diagnostic or prognosis biomarkers, as well as to design effective therapeutic means to control tumor progression. Here, we provide an overview of RNA splicing mechanisms and use prostate cancer as an example to review recent advancements in our understanding of RNA splicing in cancer progression and therapy resistance. We also discuss emerging diagnostic and therapeutic potentials of RNA splicing events or RNA splicing factors.

几乎正常细胞中的所有基因都经历了选择性 RNA 剪接，以产生更大程度的基因产物多样化，以实现正常细胞功能。RNA 剪接受到严格调控，并与遗传和表观遗传机制密切相互作用。虽然 DNA 多态性和体细胞突变调节可变剪接模式，但 RNA 剪接也控制基因组稳定性、染色质组织和转录组。反过来，肿瘤细胞经常利用异常的 RNA 剪接来发展、生长并发展为耐药性肿瘤。因此，了解肿瘤细胞中的选择性 RNA 剪接将为我们提供进一步了解肿瘤生物学、确定诊断或预后生物标志物以及设计控制肿瘤进展的有效治疗手段的机会。这里，我们提供了 RNA 剪接机制的概述，并以前列腺癌为例来回顾我们对 RNA 剪接在癌症进展和治疗抵抗中的理解方面的最新进展。我们还讨论了 RNA 剪接事件或 RNA 剪接因子的新兴诊断和治疗潜力。