GSE184784
Transcriptome of NK-92 cells with pharmacological inhibition of SUPT16H, a subunit of FACT complex, by using its inhibitor curaxin 137 (CBL0137)
Purpose: This study aims to evaluate the effect of FACT complex inhibitor CBL0137 to the total transcriptome of NK-92 cells through RNA-seq assay. Methods: NK-92 cells were treated with CBL0137 (500 nM) or DMSO for 24 h. RNA samples were extracted and submitted to GENEWIZ (South Plainfield, NJ 07080) for quality control and subsequent rRNA removal through polyA selection, followed by the library preparation. Sequencing was carried out on an Illumina HiSeq platform with the configuration of 2 × 150 bp (paired end), and > 20 million reads per sample were achieved. Differential expression of genes was analyzed by DESeq2. Results: R packages, pheatmap and clusterProfiler, were used for heatmap construction and pathway analysis, respectively. 917 genes were enriched based on the fold-change > 1.5 as well as the adjusted P-value < 0.05. GO biological process (BP) analysis shows that inteferon signaling and anti-viral responses are among top enriched pathways. Expression of interferons and interferon-stimulated genes (ISGs) are increased based on heatmap, which was further validated through quantitative reverse transcription PCR (RT-qPCR) assay. Conclusions: CBL0137 causes the systemic upregulation of IFNs and ISGs with statistical significance in NK-92 cells, which shows the potential of CBL0137 to trigger the anti-viral innate immunity. In addition, due to the upragulation of IFN-gamma pathways, CBL0137 also shows the ability to increase the NK cytotoxicity. Overall design: NK-92 cells were treated with either DMSO as a control, or CBL0137 (500 nM) for 24 h. Four independent experiments were performed. Totally 8 samples were subjected to RNA-seq assay.