Effect of p53 knockout on gene expression during capmatinib treatment of NF1-MET murine MPNST cells

To investigate the function of p53 in regulating response to MET inhibition in MPNST cells we established NF1-MET;sgP53 cells in which Trp53 was knocked out using CRISPR-Cas9. As a control, the parental NF1-MET was transduced with CRISPR-Cas9 in the absence of sgRNA. We then performed gene expression profiling analysis using data obtained from RNA-seq of the 2 different cells treated with either capmatinib or vehicle in duplicate. Comparative gene expression profiling analysis of RNA-seq data for NF1-MET cells and its Trp53 KO derivative NF1-MET;sgP53 with and without capmatinib treatment.

为探究p53在恶性外周神经鞘膜瘤（Malignant Peripheral Nerve Sheath Tumor, MPNST）细胞中调控间质上皮转化因子（MET）抑制应答的功能，我们利用成簇规律间隔短回文重复序列相关蛋白9（CRISPR-Cas9）系统敲除Trp53基因，构建了NF1-MET;sgP53细胞系。作为对照，我们将仅转导CRISPR-Cas9系统、未引入靶向单向导RNA（sgRNA）的亲本NF1-MET细胞作为对照组。随后，我们针对经卡马替尼（capmatinib）或溶剂对照（vehicle）处理的两类细胞的RNA测序（RNA-seq）数据开展基因表达谱分析，每组均设置两次生物学重复。本研究针对经卡马替尼处理与未处理的NF1-MET细胞及其Trp53敲除衍生细胞系NF1-MET;sgP53的RNA测序数据，开展对比基因表达谱分析。