PRMT5 and CDK4/6 inhibition result in distinctive patterns of alternative splicing

To investigate the full effects of inhibition of CDK4/6 on splicing events in melanoma and the extent to which they are dependent on PRMT5 . We performed full-length mRNA sequencing on CHL1 and A375 melanoma cell lines treated with the CDK4/6 inhibitor palbociclib and the PRMT5 inhibitor GSK3326595 and CTX085 and analysed data for differential gene expression and differential pre-mRNA splicing induced by these agents. Overall design: Comparative gene expression profiling analysis of RNA-seq data for CDK4/6 and PRMT5 inhibited CHL1 and A375 melanoma cells.

为探究细胞周期蛋白依赖性激酶4/6（CDK4/6）抑制对黑色素瘤细胞剪接事件的全面影响，以及此类剪接事件依赖于蛋白质精氨酸甲基转移酶5（PRMT5）的程度。本研究对经CDK4/6抑制剂帕博西尼（palbociclib）、PRMT5抑制剂GSK3326595与CTX085处理的CHL1及A375黑色素瘤细胞系开展全长mRNA测序，并针对上述药物诱导的差异基因表达与差异前体mRNA（pre-mRNA）剪接事件进行数据分析。整体实验设计：对经CDK4/6与PRMT5抑制处理的CHL1及A375黑色素瘤细胞的RNA测序（RNA-seq）数据进行比较基因表达谱分析。